Salpingitis due to Entamoeba histolytica.
(73/861)
We describe the pathology of a unique case of Fallopian tube amebiasis, associated with hydrosalpinx, in a 21-year-old woman. She complained of lower abdominal pain, had a foul-smelling green vaginal discharge and fever during one week. There was a discrete increase in body temperature and a painful abdominal palpation at the lower right side, with signs of local peritoneal irritation. Pathological examination showed a marked dilatation of the fallopian tube and hydrosalpinx. Microscopic examination showed a poorly formed granuloma composed of large macrophages with many Entamoeba histolytica trophozoites inside the fallopian tube. Even though it is a rare disease the correct diagnosis of female genital tract amebiasis is of great importance for the indication of proper therapy. (+info)
The membrane-peripheral subunits of transhydrogenase from Entamoeba histolytica are functional only when dimerized.
(74/861)
Unlike their bacterial and mammalian counterparts, the NADP(H)- and NAD(H)-binding components of proton-translocating transhydrogenase from the protozoan parasite Entamoeba histolytica (denoted ehdIII and ehdI, respectively) are tethered by a polypeptide linker. The recombinant tethered fragment, ehdIII-ehdI, was prepared without its membrane-spanning dII component. Dimers of ehdIII-ehdI catalyzed transhydrogenation, but monomers were inactive. The addition of ehdIII to ehdIII-ehdI monomers did not lead to an increase in the rate of transhydrogenation, showing that this inactivity is not the result of an unfavorable topology introduced by the linker. The addition of a bacterial dI to ehdIII-ehdI led to an increase in the rate of transhydrogenation, showing that the linker is flexible. A hybrid protein in which ehdIII is tethered to the bacterial dI (denoted ehdIII-rrdI) more readily formed active dimers. Data from small angle x-ray scattering by the hybrid dimers were fitted to models derived from the high-resolution crystal structure of the bacterial dI(2)dIII(1) complex (Cotton, N. P. J., White, S. A., Peake, S. J., McSweeney, S., and Jackson, J. B. (2001) Structure 9, 165-T176). The results show that the ehdIII-rrdI dimer is asymmetric; one dIII associates with dI, as in the bacterial complex, but the other is displaced. The results provide evidence for the alternating site, binding change model for proton translocation by intact transhydrogenase. (+info)
Fate of Entamoeba histolytica during establishment of amoebic liver abscess analyzed by quantitative radioimaging and histology.
(75/861)
The protozoan parasite Entamoeba histolytica is the causative agent of amoebiasis, a human disease characterized by dysentery and liver abscess. The physiopathology of hepatic lesions can be satisfactorily reproduced in the hamster animal model by the administration of trophozoites through the portal vein route. Hamsters were infected with radioactively labeled amoebas for analysis of liver abscess establishment and progression. The radioimaging of material from parasite origin and quantification of the number inflammation foci, with or without amoebas, described here provides the first detailed assessment of trophozoite survival and death during liver infection by E. histolytica. The massive death of trophozoites observed in the first hours postinfection correlates with the presence of a majority of inflammatory foci without parasites. A critical point for success of infection is reached after 12 h when the lowest number of trophozoites is observed. The process then enters a commitment phase during which parasites multiply and the size of the infection foci increases fast. The liver shows extensive areas of dead hepatocytes that are surrounded by a peripheral layer of parasites facing inflammatory cells leading to acute inflammation. Our results show that the host response promotes massive parasite death but also suggest also that this is a major contributor to the establishment of inflammation during development of liver abscess. (+info)
The Jacob lectin, the most abundant glycoprotein in the cyst wall of Entamoeba invadens, contains five unique 6-Cys chitin-binding domains (CBDs). We identified Entamoeba histolytica and Entamoeba dispar genes encoding Jacob homologues, each of which contains two predicted 6-Cys CBDs. A unique 8-Cys CBD was found at the N termini of the E. histolytica chitinase and three other predicted lectins, called Jessie 1 to Jessie 3. The CBDs of four E. histolytica lectins (Jacob, chitinase, and Jessies 2 and 3) were expressed in secretory vesicles of transfected amebae and shown to bind to particulate chitin. (+info)
Innate and acquired resistance to amebiasis in bangladeshi children.
(77/861)
Entamoeba histolytica infection and colitis occurred in 55% and 4%, respectively, of a cohort of Bangladeshi preschool children observed for 2 years. DNA typing demonstrated that infecting E. histolytica isolates were genetically diverse. Innate resistance to infection in children was linked to the absence of serum anti-trophozoite IgG. Most children who lacked serum anti-trophozoite IgG failed to develop it in response to a new infection. The serum anti-trophozoite IgG response clustered in families, which is consistent with genetic inheritance. Acquired resistance to infection was linked to intestinal IgA against the carbohydrate-recognition domain of the E. histolytica galactose N-acetyl-d-galactosamine lectin. This was associated with an 86% reduction in new infection over 1 year. Amebiasis is a common and potentially serious infection in children from Dhaka, and both innate and acquired immune responses limit infection. (+info)
Differentiation of entamoeba histolytica/entamoeba dispar by PCR and their correlation with humoral and cellular immunity in individuals with clinical variants of amoebiasis.
(78/861)
To correlate a particular state of immunity with Entamoeba spp., we used colorimetric PCR to differentiate E. histolytica from E. dispar in individuals with amoebiasis and to associate its presence with the clinical profile, including humoral and cellular immune responses to E. histolytica. Our results showed high levels of antibody in acute amoebiasis and elevation of IL-4 production, a cytokine related to Th2 profile, associated with E. histolytica. In chronic amoebiasis, even with anti-E. histolytica seropositivity, intestinal symptoms were associated with E. dispar in all the cases, without differences in level of antibodies, BTI, CD4+/CD8+ ratio, INF-gamma, and IL-4. Among asymptomatic carriers, E. dispar was more frequently found; however, identification of E. histolytica in two asymptomatic carriers associated with high levels of INF-gamma, a cytokine related to Th1 profile, demonstrate the importance of making specific diagnosis of Entamoeba spp., to establish the clinical and epidemiological behavior in both intestinal and extra-intestinal amoebiasis. (+info)
A monoclonal antibody to the amebic lipophosphoglycan-proteophosphoglycan antigens can prevent disease in human intestinal xenografts infected with Entamoeba histolytica.
(79/861)
Entamoeba histolytica trophozoites are covered by lipophosphoglycan-peptidoglycan molecules which may be key virulence factors. We found that pretreatment of severe combined immunodeficient mice bearing human intestinal xenografts with a monoclonal antibody to the amebic lipophosphoglycan-peptidoglycan molecules can prevent or significantly reduce the human intestinal inflammation and tissue damage that are normally seen with E. histolytica colonic infection. (+info)
The mouse model of amebic colitis reveals mouse strain susceptibility to infection and exacerbation of disease by CD4+ T cells.
(80/861)
Amebic colitis is an important worldwide parasitic disease for which there is not a well-established animal model. In this work we show that intracecal inoculation of Entamoeba histolytica trophozoites led to established infection in 60% of C3H mice, while C57BL/6 or BALB/c mice were resistant, including mice genetically deficient for IL-12, IFN-gamma, or inducible NO synthase. Infection was a chronic and nonhealing cecitis that pathologically mirrored human disease. Characterization of the inflammation by gene chip analysis revealed abundant mast cell activity. Parasite-specific Ab and cellular proliferative responses were robust and marked by IL-4 and IL-13 production. Depletion of CD4(+) cells significantly diminished both parasite burden and inflammation and correlated with decreased IL-4 and IL-13 production and loss of mast cell infiltration. This model reveals important immune factors that influence susceptibility to infection and demonstrates for the first time the pathologic contribution of the host immune response in amebiasis. (+info)