| pubmed-article:12660071 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12660071 | lifeskim:mentions | umls-concept:C0002438 | lld:lifeskim |
| pubmed-article:12660071 | pubmed:issue | 9362 | lld:pubmed |
| pubmed-article:12660071 | pubmed:dateCreated | 2003-3-27 | lld:pubmed |
| pubmed-article:12660071 | pubmed:abstractText | Amoebiasis is the second leading cause of death from parasitic disease worldwide. The causative protozoan parasite, Entamoeba histolytica, is a potent pathogen. Secreting proteinases that dissolve host tissues, killing host cells on contact, and engulfing red blood cells, E histolytica trophozoites invade the intestinal mucosa, causing amoebic colitis. In some cases amoebas breach the mucosal barrier and travel through the portal circulation to the liver, where they cause abscesses consisting of a few E histolytica trophozoites surrounding dead and dying hepatocytes and liquefied cellular debris. Amoebic liver abscesses grow inexorably and, at one time, were almost always fatal, but now even large abscesses can be cured by one dose of antibiotic. Evidence that what we thought was a single species based on morphology is, in fact, two genetically distinct species--now termed Entamoeba histolytica (the pathogen) and Entamoeba dispar (a commensal)--has turned conventional wisdom about the epidemiology and diagnosis of amoebiasis upside down. New models of disease have linked E histolytica induction of intestinal inflammation and hepatocyte programmed cell death to the pathogenesis of amoebic colitis and amoebic liver abscess. | lld:pubmed |
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| pubmed-article:12660071 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12660071 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12660071 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12660071 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12660071 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:12660071 | pubmed:issn | 0140-6736 | lld:pubmed |
| pubmed-article:12660071 | pubmed:author | pubmed-author:StanleySamuel... | lld:pubmed |
| pubmed-article:12660071 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12660071 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:12660071 | pubmed:volume | 361 | lld:pubmed |
| pubmed-article:12660071 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12660071 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12660071 | pubmed:pagination | 1025-34 | lld:pubmed |
| pubmed-article:12660071 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:12660071 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12660071 | pubmed:articleTitle | Amoebiasis. | lld:pubmed |
| pubmed-article:12660071 | pubmed:affiliation | Department of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO, St Louis, MO 63110, USA. sstanley@im.wustl.edu | lld:pubmed |
| pubmed-article:12660071 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12660071 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:12660071 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:12660071 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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