Overview

Brief Summary

Although several protozoan species in the genus Entamoeba colonize humans, not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic amoeba causing amebiasis, which can involve both intestinal and extraintestinal infections. The other Entamoeba species are important because they may be confused with E. histolytica in diagnostic investigations. Two morphologically identical but genetically distinct and apparently largely nonpathogenic species, E. dispar and E. moshkovskii, are now believed to account for most asymptomatic Entamoeba infections in humans (Pritt and Clark 2008).

Entamoeba histolytica has a worldwide distribution, with a higher incidence of amebiasis in developing countries. Risk groups in industrialized countries include homosexual males, travelers and recent immigrants (although disease may develop months to years after exposure), and institutionalized populations. Infection by E. histolytica typically occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Cysts can survive for days to weeks in the external environment. Transmission can also occur through exposure to fecal matter during sexual contact (in this case not only cysts but also the far less durable trophozoite stage could prove infective). (Source: Centers for Disease Control Parasites and Health website)

Entamoeba histolytica is responsible for an estimated 35 to 50 million cases of symptomatic disease and around 100,000 deaths annually, apparently as a result of parasite destruction of host tissue. The majority of morbidity and mortality occurs in Asia, Central and South America, and Africa. Children are especially vulnerable as they can suffer from malnourishment and stunted growth as a result of repeated infection. (Ralston and Petri 2011 and references therein)

Entamoeba hemolytica are generally considered to be anaerobic since they can be grown in vitro only under conditions of reduced oxygen tension. However, metabolically these parasitic protozoa have been found to be microaerobic or microaerophilic, consuming oxygen to a certain extent and produce toxic oxygen derivatives. Given this fact, it is notable that they lack some or all of the usual antioxidant defense mechanisms present in aerobic and other aerotolerant cells, a phenomenon reviewed and discussed by Tekwani and Mehlotra (1999).



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Distribution

Entamoeba histolytica has a worldwide distribution, with a higher incidence of amebiasis in developing countries. Risk groups in industrialized countries include homosexual males, travelers and recent immigrants (although disease may develop months to years after exposure), and institutionalized populations.The majority of morbidity and mortality occurs in Asia, Central and South America, and Africa.

(Centers for Disease Control Parasites and Health website; Ralston and Petri 2011 and references therein)

  • Ralston, K. S. and W.A. Petri. 2011. Tissue destruction and invasion by Entamoeba histolytica. Trends in Parasitology. 27(6): 253-262.
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Life History and Behavior

Life Cycle

Infection by E. histolytica typically occurs by ingestion of mature cysts in fecally contaminated food, water, or hands. Cysts can survive for days to weeks in the external environment. Transmission can also occur through exposure to fecal matter during sexual contact (in this case not only cysts but also the far less durable trophozoite stage could prove infective).

(Centers for Disease Control Parasites and Health website)

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Physiology and Cell Biology

Physiology

Entamoeba hemolytica are generally considered to be anaerobic since they can be grown in vitro only under conditions of reduced oxygen tension. However, metabolically these parasitic protozoa have been found to be microaerobic or microaerophilic, consuming oxygen to a certain extent and produce toxic oxygen derivatives. Given this fact, it is notable that they lack some or all of the usual antioxidant defense mechanisms present in aerobic and other aerotolerant cells, a phenomenon reviewed and discussed by Tekwani and Mehlotra (1999).

  • Tekwani, B.L. and R.K. Mehlotra. 1999. Molecular basis of defence against oxidative stress in Entamoeba histolytica and Giardia lamblia. Microbes and Infection. 1(5): 385-394.
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Relevance to Humans and Ecosystems

Risks

Although several protozoan species in the genus Entamoeba colonize humans, not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic amoeba causing amebiasis, which can involve both intestinal and extraintestinal infections. The other Entamoeba species are important because they may be confused with E. histolytica in diagnostic investigations.

Entamoeba histolytica is responsible for an estimated 35 to 50 million cases of symptomatic disease and around 100,000 deaths annually, apparently as a result of parasite destruction of host tissue. The majority of morbidity and mortality occurs in Asia, Central and South America, and Africa. Children are especially vulnerable as they can suffer from malnourishment and stunted growth as a result of repeated infection.

(Pritt and Clark 2008 and references therein; Ralston and Petri 2011 and references therein)

  • Pritt, B. S. and C.G. Clark. 2008. Amebiasis. Mayo Clinic Proceedings. 83, 1154-1160.
  • Ralston, K. S. and W.A. Petri. 2011. Tissue destruction and invasion by Entamoeba histolytica. Trends in Parasitology. 27(6): 253-262.
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Wikipedia

Entamoeba histolytica

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.

Transmission[edit]

The active (trophozoite) stage exists only in the host and in fresh loose feces; cysts survive outside the host in water, in soils, and on foods, especially under moist conditions on the latter. The cysts are readily killed by heat and by freezing temperatures, and survive for only a few months outside of the host.[3] When cysts are swallowed they cause infections by excysting (releasing the trophozoite stage) in the digestive tract. The pathogenic nature of E. histolytica was first reported by Lösch in 1875, but it was not given its Latin name until Fritz Schaudinn described it in 1903. E. histolytica, as its name suggests (histolytic = tissue destroying), is pathogenic; infection can be asymptomatic or can lead to amoebic dysentery or amoebic liver abscess.[1] Symptoms can include fulminating dysentery, bloody diarrhea, weight loss, fatigue, abdominal pain, and amoeboma. The amoeba can actually 'bore' into the intestinal wall, causing lesions and intestinal symptoms, and it may reach the blood stream. From there, it can reach different vital organs of the human body, usually the liver, but sometimes the lungs, brain, spleen, etc. A common outcome of this invasion of tissues is a liver abscess, which can be fatal if untreated. Ingested red blood cells are sometimes seen in the amoeba cell cytoplasm.

Genome[edit]

The E. histolytica genome was sequenced, assembled, and automatically annotated in 2005.[4] The genome was reassembled and reannotated in 2010.[5] 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.[6] The major group of transposable elements in E. histlytica are non-LTR retrotransposons. These have been divided in three families called EhLINEs and EhSINEs (EhLINE1,2,3 and EhSINE1,2,3).[7] 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.[8]

Pathogen interaction[edit]

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.[9] 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.[10]

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.[11]

Diagnosis[edit]

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.

Treatment[edit]

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 nitroimidazole derivatives are used because they are highly effective against the trophozoite form of the amoeba. Since they have little effect on amoeba cysts, usually this treatment is followed by an agent (such as paromomycin or diloxanide furoate) that acts on the organism in the 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.[12]

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 SpeciesEntamoeba histolytica
Etiologic Agent of:Amoebiasis; Amoebic dysentery; Extraintestinal Amoebiasis, usually Amoebic Liver Abscess = “anchovy sauce”); Amoeba Cutis; Amoebic Lung Abscess (“liver-colored sputum”)
Infective stageTetranucleated cyst (having 4 nuclei)
Definitive HostHuman
Portal of EntryMouth
Mode of TransmissionIngestion of mature cyst through contaminated food or water
HabitatColon and Cecum
Pathogenic StageTrophozoite
Locomotive apparatusPseudopodia (“False Foot”)
MotilityActive, Progressive and Directional
Nucleus'Ring and dot' appearance: peripheral chromatin and central karyosome
Mode of ReproductionBinary Fission
PathogenesisLytic necrosis (it looks like “flask-shaped” holes in Gastrointestinal tract sections (GIT)
Type of EncystmentProtective and Reproductive
Lab DiagnosisMost 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
TreatmentMetronidazole 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.[13] 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.[14][15]
Trophozoite Stage
Pathognomonic/Diagnostic FeatureIngested RBC; distinctive nucleus
Cyst Stage
Chromatoidal Body'Cigar' shaped bodies (made up of crystalline ribosomes)
Number of Nuclei1 in early stages, 4 when mature
Pathognomonic/Diagnostic Feature'Ring and dot' nucleus and chromatoid bodies

Additional images[edit]

See also[edit]

References[edit]

  1. ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 733–8. ISBN 0-8385-8529-9. 
  2. ^ "Amoebiasis". Wkly. Epidemiol. Rec. 72 (14): 97–9. April 1997. PMID 9100475. 
  3. ^ American Water Works Association (June 2006). Waterborne Pathogens. American Water Works Association. ISBN 978-1-58321-403-9. 
  4. ^ 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.
  5. ^ 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.
  6. ^ Caler, E and Lorenzi, H (2010). "Entamoeba histolytica: Genome Status and Web Resources". Anaerobic Parasitic Protozoa: Genomics and Molecular Biology. Caister Academic Press. ISBN 978-1-904455-61-5. 
  7. ^ 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. doi:10.1016/j.exppara.2005.02.009. 
  8. ^ 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. doi:10.1111/j.1742-4658.2009.07419.x. PMID 19878305. 
  9. ^ 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. doi:10.1001/archinte.165.4.409. PMID 15738369. 
  10. ^ 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. doi:10.1097/00002030-199101000-00014. PMID 2059366. 
  11. ^ 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. PMC 356300. PMID 4335522. 
  12. ^ Kucik, CJ; Martin, GL, Sortor, BV (Mar 1, 2004). "Common intestinal parasites.". American family physician 69 (5): 1161–8. PMID 15023017. 
  13. ^ Blessmann J, Tannich E (October 2002). "Treatment of asymptomatic intestinal Entamoeba histolytica infection". N. Engl. J. Med. 347 (17): 1384. doi:10.1056/NEJM200210243471722. PMID 12397207. 
  14. ^ Stanley SL (March 2003). "Amoebiasis". Lancet 361 (9362): 1025–34. doi:10.1016/S0140-6736(03)12830-9. PMID 12660071. 
  15. ^ "Diloxanide (Systemic)". Retrieved 17 November 2011. 
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