Introduction: An amebic liver abscess is the most common presentation of extraintestinal amebiasis. This condition is the result of a parasite infection caused by Entamoeba histolytica. Materials and Methods: We report a case of a 53-year-old male who presented with abdominal pain in the right upper quadrant, jaundice, and a 10-kg weight loss within a 1-month span. Results and Conclusion: A wide range of symptoms and findings in the imaging tests suggestive of neoplasia, elevated levels of CA 19-9 and CA 125, and the presentation of biliary peritonitis as a complication makes this case a challenge for its approach and management. / Revisión por pares

Entamoeba histolytica is the protozoan parasite that causes amoebic dysentery and amoebic liver abscesses in humans. For many years it was believed to be a primitive organism because it lacks many typical eukaryotic features including mitochondria. Recently, two genes that in other organisms encode proteins normally found in the mitochondrion have been isolated, giving evidence for the secondary loss of mitochondrial function in E. histolytica. These are the pyridine nucleotide transhydrogenase (PNT) and the mitochondrial chaperonin cpn60 genes. In this study we isolated and characterised a gene encoding a mitochondrial-type heat shock protein 70 from E. histolytica. cDNA and genomic library clones have been isolated and sequenced. Comparison with previously published sequences confirmed the assumption that E. histolytica comes from mitochondrion - bearing ancestors. Southern blot hybridisation revealed there are two copies of the gene in the genome. Northern blot analysis revealed two transcripts hybridising to the mt-hsp70 probe that differ in length and which are induced by heat shock. In addition, an apparently noncoding, polyadenylated RNA that is also induced by heat shock is encoded immediately upstream of the mitochondrial-type hsp70 gene. Expression analysis was also performed in four other Entamoeba species. Partial cpn60, PNT, and mt-hsp70 genes were isolated and the size of the mRNAs and their heat shock induction levels were investigated by hybridisation to these probes. The similarity of the mt-hsp70 amino terminus to those of hydrogenosomal proteins in conjunction with the phylogenetic analyses suggests it is also likely to be targeted to the mitochondrion-derived organelle of E. histolytica known as the mitosome.

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Entamoeba histolytica is a protozoan parasite and the causative agent of amoebiasis. While infection is associated with suppression of cell-mediated, immunity, drug-cured patients are resistant to reinvasion by amoebae. Macrophages are the principal effector cells in host defence against E. histolytica via production of nitric oxide which is cytotoxic for the parasite. The objective of this study was to determine the T cell cytokine responses associated with host defence against E. histolytica . A mixed Th1/Th2 (Th0) response predominated at days 5--10 of amoebic liver abscess development in gerbils, as indicated by spleen and hepatic lymph node cell IL-2 (Th1 marker) and IL-4 (Th2 marker) production. However, T cell responses were profoundly suppressed at day 20 of infection. Serum collected at day 20, but not at other times, markedly suppressed T cell proliferative responses by inhibiting IL-2 production. A switch to a Th1 response occurred after day 20 of infection. Following drug-abbreviation of infection at day 20, animals were completely resistant to challenge infection in the liver and demonstrated a Th1 response. The Gal-lectin 170-kDa heavy subunit of E. histolytica is a protective antigen in gerbils and a potential subunit vaccine candidate. We determined which region of the Gal-lectin stimulates IL-12 production, as IL-12 is key to inducing Th1 cytokine responses. Native Gal-lectin plus interferon-gamma stimulated IL-12 p40 and p35 gene transcription and IL-12 p70 protein production in human macrophages. Using a panel of anti-170-kDa subunit monoclonal antibodies in inhibition studies, aa 596--998 was identified as the IL-12-inducing domain. These results suggest that this portion of the Gal-lectin has potential for use as a subunit vaccine to induce Th1-mediated immunity against E. histolytica .

Infections with Entamoeba histolytica are associated with impaired cell mediated immunity by an unknown mechanism. Macrophages are the most important cells in host defense against invasive amebiasis. The present study investigated the effect of E. histolytica on macrophage functions. Macrophages isolated from gerbils with amebic liver abscess and naive macrophages exposed to soluble amebic proteins induced profound alteration of eicosanoid formation both in cyclooxygenase and lipoxygenase pathways by enhanced PGE$ sb2$ and LTC$ sb4$ production. TNF-$ alpha$ production by macrophages was altered locally in amebic granulomas and at systemic sites during the infection and in response to amebic proteins stimulation in vitro. PGE$ sb2$ produced by macrophages in response to amebic proteins was involved in the down-regulation of TNF-$ alpha$ production. E. histolytica-induced dysfunction of macrophage cytotoxicity against amebae and tumor cells occurred by suppressing NO and by enhancing PGE$ sb2$ production. Amebic proteins suppressed the induction. of IFN-$ gamma$-induced bone marrow macrophage class II MHC Ia molecule synthesis and I-A$ beta$ mRNA expression by stimulating PGE$ sb2$ production. Taken together, these results demonstrate that E. histolytica induced PGE$ sb2$ production plays a central role in the suppression of macrophage effector and accessory cell functions.

Entamoeba histolytica is a protozoan parasite and the causative agent of amebiasis. Activated macrophages are the main host effector cells in host defence against E. histolytica, through the production of nitric oxide (NO) which is cytotoxic for the parasite. NO is upregulated by tumor necrosis factor-alpha (TNF-$ alpha$) produced by macrophages. The objective of this study was to determine the effect of amebic components on TNF-$ alpha$ and NO production by macrophages. Soluble E. histolytica proteins stimulated naive macrophages for enhanced TNF-$ alpha$ mRNA expression through PKC signal transduction. E. histolytica-induced TNF-$ alpha$ mRNA expression was unstable, and macrophages pretreated with E. histolytica proteins expressed reduced levels of TNF-$ alpha$ mRNA in response to LPS or IFN-$ gamma$ + LPS. In contrast, the purified galactose-adherence lectin (Gal-lectin) of E. histolytica stimulated naive macrophages for stable TNF-$ alpha$ mRNA expression and protein production. Furthermore, IFN-$ gamma$ primed macrophages produced TNF-$ alpha$ and NO in response to the Gal-lectin. Naive macrophages exposed to Gal-lectin + IFN-$ gamma$ were activated to kill E. histolytica trophozoites in vitro by NO. Anti-lectin monoclonal antibodies that recognize non-overlapping epitopes of the kDa heavy subunit of the Gal-lectin identified amino acids 596-1082 as important in mediating amebic adherence to target cells and TNF-$ alpha$ mRNA induction in macrophages. Likewise, a region between amino acids 596-818 of the 170 kDa Gal-lectin, in conjunction with IFN-$ gamma$, activated macrophages for TNF-$ alpha$ and NO production and amebicidal activity. This research demonstrates the immunogenic potential of the E. histolytica Gal-lectin and the critical regions that could be used as a subunit vaccine candidate against amebiasis.

Thesis (Ph. D.)--University of Virginia, 1998. / Spine title: CRD of the E. histolytica Gall lectin. Includes bibliographical references (p. 71-87). Also available online through Digital Dissertations.

Thesis (Ph.D.)—Boston University / Endamoeba histolytica, the etiological agent of amoebiasis, was first cultivated in the presence of associated bacteria by Boeck and Drbohlav (Am. J. Hyg., 5: 371-407, 1925). Since that time numerous workers have attempted to culture the amebas free of bacteria but have been unsuccessful. The majority of studies on the cultural requirements of this protozoan has been complicated by the presence of more than one species of bacteria. Therefore, the nutritional studies on E. histolytica have been very meager. A pure culture of this organism is essential to the elucidation of its metabolism, physiology, and immunology. It was the purpose of this investigation to identify growth factors required by the amebas so that a pure culture may become available. In order to control the associated bacteria during the assay of growth factors, penicillin and streptomycin were added to the culture medium in high concentrations. This concentration of the antibiotics was shown to sterilize the bacterial flora yet have no detrimental effect on the amebas. Many compounds were tested for their ameba-growth-promoting activity under bacteria free conditions. The test medium consisted of egg slants over-layed with normal horse serum in Ringer solution, dextrose, sodium thioglycollate, rice starch, antibiotics and a vaspar anaerobic seal [TRUNCATED]

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