Explore the vast range of titles available.

Entamoeba histolytica is the responsible parasite of amoebiasis and remains one of the top three parasitic causes of mortality worldwide. With increased travel and emigration to developed countries, infection is becoming more common in nonendemic areas. Although the majority of individuals infected with E. histolytica remain asymptomatic, some present with amoebic colitis and disseminated disease. As more is learned about its pathogenesis and the host’s immune response, the potential for developing a vaccine holds promise. This narrative review outlines the current knowledge regarding E. histolytica and E. dispar and insight in the development of a vaccine.

Background Parasitic infections, particularly those caused by protozoa, represent a considerable public health problem in developing countries. Blastocystis , Giardia duodenalis , Cryptosporidium spp. and the Entamoeba complex ( Entamoeba histolytica, Entamoeba dispar and Entamoeba moshkovskii) are the most common etiological causes of intestinal parasitic infections. Methods We carried out a descriptive cross-sectional study in school-age children attending a daycare institution in commune eight of Popayán, Cauca (Southwest Colombia). A total of 266 fecal samples were collected (258 from children and eight from pets). Blastocystis , G. duodenalis , Cryptosporidium spp. and the Entamoeba complex were identified by microscopy, quantitative real-time PCR (qPCR) and conventional PCR. The concordance of qPCR and microscopy was assessed using the Kappa index. Molecular characterization was conducted to identify Blastocystis subtypes (18S), G. duodenalis assemblages ( tpi and gdh ) and Cryptosporidium species/subtypes (18S and GP60). Potential associations between intestinal parasitism and sociodemographic factors were examined using bivariate analyses. Results A total of 258 fecal samples from children were analyzed by microscopy and 255 samples were analyzed by qPCR. The prevalence of Blastocystis was between 25.19% (microscopy) and 39.22% (qPCR), that of G. duodenalis was between 8.14% (microscopy) and 10.59% (qPCR), that of Cryptosporidium spp. was estimated at 9.8% (qPCR), and that of the Entamoeba complex was between 0.39% (conventional PCR) and 0.78% (microscopy). The concordance between microscopy and qPCR was very low. Blastocystis ST1 (alleles 4, 8, and 80), ST2 (alleles 11, 12, and 15), ST3 (alleles 31, 34, 36, 38,57, and 151), and ST4 (alleles 42 and 91), G. duodenalis assemblages AII, BIII, BIV and D, C. parvum subtype IIa and C. hominis subtype IbA9G3R2 were identified. The only identified member of the Entamoeba complex corresponded to E. histolytica . No statistically significant association was identified between parasitic infection and any sociodemographic variable. Conclusion This study revealed the usefulness of molecular methods to depict the transmission dynamics of parasitic protozoa in southwest Colombia. The presence of some of these protozoa in domestic animals may be involved in their transmission.

Amebiasis is a parasitic infection of the human intestines, primarily caused by Entamoeba histolytica . Its pathogenesis relies on the environmental sensing-induced cytoskeletal remodeling as the basic mechanism for motility and tissue invasion. We identified and characterized an atypical Venus Fly-Trap (VFT) receptor protein, Eh VFT (CL6EHI_096680). While it shares homology with the ligand-binding domain of class C GPCRs, it is phylogenetically related to the Periplasmic Binding Protein (PBP) superfamily. This protein is uniquely lacking a transmembrane domain. Instead, the glycosylphosphatidylinositol (GPI) anchor is responsible for its cell membrane localization. Removal of the GPI signal led to unexpected mitosomal localization, highlighting the importance of GPI modification in subcellular targeting. Functional studies revealed that Eh VFT knockdown reduced parasite motility and phagocytosis of mammalian cells following the reduction of expression of actin cytoskeleton-related genes, including myosin II, villidin, and gelsolin. Our findings suggest that Eh VFT plays a role in regulating downstream signaling linked to Entamoeba motility and phagocytosis. This study provides novel insights into an atypical VFT protein in E. histolytica , an area previously understudied.

Entamoeba histolytica , the causative agent of fatal diarrhoeal disease in children in the developing world, is shown here to kill human cells by biting off and ingesting pieces of cells, in a process reminiscent of the trogocytosis seen between immune cells; ingestion of bites is required for killing and this mechanism is used both in tissue culture and during invasion of intestinal explants. Entamoeba take a bite of intestine Entamoeba histolytica , the causative agent of fatal diarrhoeal disease in children in the developing world, was so named for its ability to destroy host tissues, although the mechanism underlying this effect was unclear. Here Katherine Ralston et al . describe how these amoeba kill intestinal epithelial cells by biting off and ingesting pieces of cell, in a process reminiscent of the trogocytosis seen between immune cells. Ingestion of the bites is required for killing, and the mechanism operates both in tissue culture and during invasion of intestinal explants. The authors suggest that intercellular exchange via trogocytosis may be more evolutionarily ancient and widespread than was assumed. This work also highlights amoebic trogocytosis as a potential target for new drugs to treat amoebiasis — a major neglected disease. Entamoeba histolytica is the causative agent of amoebiasis, a potentially fatal diarrhoeal disease in the developing world. The parasite was named “ histolytica ” for its ability to destroy host tissues, which is probably driven by direct killing of human cells. The mechanism of human cell killing has been unclear, although the accepted model was that the parasites use secreted toxic effectors to kill cells before ingestion 1 . Here we report the discovery that amoebae kill by ingesting distinct pieces of living human cells, resulting in intracellular calcium elevation and eventual cell death. After cell killing, amoebae detach and cease ingestion. Ingestion of human cell fragments is required for cell killing, and also contributes to invasion of intestinal tissue. The internalization of fragments of living human cells is reminiscent of trogocytosis (from Greek trogo , nibble) observed between immune cells 2 , 3 , 4 , 5 , 6 , but amoebic trogocytosis differs because it results in death. The ingestion of live cell material and the rejection of corpses illuminate a stark contrast to the established model of dead cell clearance in multicellular organisms 7 . These findings change the model for tissue destruction in amoebiasis and suggest an ancient origin of trogocytosis as a form of intercellular exchange.

Entamoeba (E.) histolytica is a major global health concern as the causative agent of amoebic colitis, yet research is hindered by the lack of an ideal animal model. While E. muris has been traditionally considered non-pathogenic, our study demonstrates that it induces a colitis-like pathology in BALB/c mice, making it a promising model for studying E. histolytica infection. Using a fecal-oral infection route, we confirmed successful E. muris colonization, leading to colonic inflammation characterized by early CD4 + T-cell infiltration and FOXP3 + regulatory T-cell recruitment. We further demonstrate that T-cell immunity is essential for E. muris colonization, as T-cell-depleted BALB/c mice and T-cell-deficient BALB/c nude mice failed to support persistent infection. Additionally, infection disrupts epithelial homeostasis, impairing goblet cell generation, and induces significant shifts in gut microbiota composition, notably reducing beneficial Firmicutes species. Collectively, these findings demonstrate that E. muris infection induces inflammation and microbiota alterations, mirroring critical aspects of amoebic colitis, reinforcing its value as a model for studying E. histolytica pathogenesis and host–parasite interactions.

Entamoeba moshkovskii is historically considered nonpathogenic. We report a case of severe extraintestinal infection in a patient from eastern India who had abdominal pain, fever, weight loss, anemia, and a splenic abscess. Molecular analysis confirmed E. moshkovskii as the causative agent. This case highlights this parasite's potential to cause severe illness.

This review article summarizes the history of amoebic dysentery (entamoebiasis) caused by Entamoeba histolytica . Initially, Entamoeba species were thought to be the most primitive extant eukaryotes, but more recent research revealed that they emerged relatively late in evolutionary history. Paleoparasitological data suggest that E. histolytica has been a parasite of humans since ancient times and was probably spread throughout the world by man during early human migration. By the end of the 19th century, it was established that E. histolytica was the etiological agent of amoebic dysentery and liver abscess. The issue over pathogenic and non-pathogenic strains of E. histolytica was resolved in the 1980s by the discovery of the morphologically indistinguishable harmless sister species Entamoeba dispar . Being mainly a disease of tropical and subtropical low-income countries, entamoebiasis cases have increased among travellers and immigrants arriving from endemic regions in recent years.

Background. An estimated 1 million children die each year before their fifth birthday from diarrhea. Previous population-based surveys of pediatric diarrheal diseases have identified the protozoan parasite Entamoeba histolytica, the etiological agent of amebiasis, as one of the causes of moderate-to-severe diarrhea in sub-Saharan Africa and South Asia. Methods. We prospectively studied the natural history of E. histolytica colonization and diarrhea among infants in an urban slum of Dhaka, Bangladesh. Results. Approximately 80% of children were infected with E. histolytica by the age of 2 years. Fecal anti-galactose/N-acetylgalactosamine lectin immunoglobulin A was associated with protection from reinfection, while a high parasite burden and expansion of the Prevotella copri level was associated with diarrhea. Conclusions. E. histolytica infection was prevalent in this population, with most infections asymptomatic and diarrhea associated with both the amount of parasite and the composition of the microbiota.

Entamoeba histolytica , a protozoan parasite, causes amebiasis. Amebiasis is mainly transmitted by oral ingestion of cysts. Cysts are produced in the large intestine of humans from proliferative trophozoites by a cell differentiation process called encystation. The Entamoeba cyst wall consists of chitins and proteins that include chitinase and Jacob and Jessie lectins. During encystation, these components are synthesized and layered around encysting Entamoeba cells. The structures of these components are well studied; however, the detailed timings of their synthesis (the transcription of the encoding genes and the translation of the resulting mRNAs) and of changes in their localization during encystation are poorly understood. Here, we performed quantitative RT-PCR and an approach combining western blotting and immunofluorescence, confocal, and immunoelectron microscopy to analyze Entamoeba invadens cells that were sampled with short-time intervals during encystation. A chitinase inhibitor, D-B-09, which disrupts the compression of chitin fibers was used to analyze component interaction with chitin fibers. All genes encoding cyst wall proteins were stage-specifically transcribed and translated, and post-translationally modified forms of Jacob1/3 were trafficked to the cyst wall before Jessie3a and Chitinase1/4 were simultaneously localized in the cyst wall. The trafficking of Jacob lectins to the cyst wall and their co-localization with chitin fibers in encysting cells were not affected by D-B-09, while the localization of Jessie protein was impaired, indicating that localizations of Jacob and Jessie lectins are spatially different positions via different modes in cyst wall. These results indicate that cyst wall components are functionally linked and that they play different roles during Entamoeba cyst wall formation. Immunoelectron microscopy confirmed the immunofluorescence and confocal microscopy results. Importantly, immunoelectron microscopy also indicated that the Entamoeba cyst wall consists of a biphasic structure of electron-light (inner) and electron-dense (outer) areas.

Entamoeba histolytica is a protozoan parasite belonging to the phylum Amoebozoa that causes amebiasis, a global public health problem. E . histolytica alternates its form between a proliferative trophozoite and a dormant cyst. Trophozoite proliferation is closely associated with amebiasis symptoms and pathogenesis whereas cysts transmit the disease. Drugs are available for clinical use; however, they have issues of adverse effects and dual targeting of disease symptoms and transmission remains to be improved. Development of new drugs is therefore urgently needed. An untargeted lipidomics analysis recently revealed structural uniqueness of the Entamoeba lipidome at different stages of the parasite’s life cycle involving very long (26–30 carbons) and/or medium (8–12 carbons) acyl chains linked to glycerophospholipids and sphingolipids. Here, we investigated the physiology of this unique acyl chain diversity in Entamoeba , a non-photosynthetic protist. We characterized E . histolytica fatty acid elongases (EhFAEs), which are typically components of the fatty acid elongation cycle of photosynthetic protists and plants. An approach combining genetics and lipidomics revealed that EhFAEs are involved in the production of medium and very long acyl chains in E . histolytica . This approach also showed that the K3 group herbicides, flufenacet, cafenstrole, and fenoxasulfone, inhibited the production of very long acyl chains, thereby impairing Entamoeba trophozoite proliferation and cyst formation. Importantly, none of these three compounds showed toxicity to a human cell line; therefore, EhFAEs are reasonable targets for developing new anti-amebiasis drugs and these compounds are promising leads for such drugs. Interestingly, in the Amoebazoan lineage, gain and loss of the genes encoding two different types of fatty acid elongase have occurred during evolution, which may be relevant to parasite adaptation. Acyl chain diversity in lipids is therefore a unique and indispensable feature for parasitic adaptation of Entamoeba .