The relation of toddy (palm wine) intake to amoebic liver abscess in a predominantly toddy-drinking population: a cross-sectional study.

The role of toddy (palm wine) as an independent risk factor for amoebic liver abscess (ALA) is not clear. In a cross-sectional study, the clinico-demographic profiles of inpatients with ALA were examined. Microscopy examination of toddy (n = 43) samples was performed. A total of 198 patients with ALA were enrolled, most of whom were: admitted during the May-August months (48%); chronic alcoholic (85% [70% toddy]); malnourished (85%); and of low socioeconomic status (88%). Clinical and laboratory parameters were comparable between toddy and distilled alcohol drinkers. None of the toddy samples revealed presence of cysts and trophozoites of Entamoeba histolytica.

[Amoebosis: May sexual transmission be an underestimated way of contamination?] / Amibiase : au cours de rapports sexuels, un mode de transmission sous-estimé ?

INTRODUCTION: Amoebiasis is a cosmopolitan disease and the third most deadly of parasitic diseases. Entamoeba histolytica is the only one to be pathogenic. Its transmission is not only related to the faecal peril but also sexual, with cases described among men who have sex with men. A case of unusual sexual transmission is described in this article, aiming to discuss the impact of these ways of transmitting amoebiasis on patient management. CASE REPORT: We describe the case of an amebic liver abscess in a 27-years-old man who did not travel in endemic areas. After patient interrogation, it seems that the contamination mode was sexual, related to a heterosexual relationship with a new female partner 4 months before the diagnosis. HIV and hepatitis B serologies were negative. CONCLUSION: The diagnosis of amoebiasis should be suspected in case of dysentery or liver abscess even if there is no history of travel in endemic areas or of sexual intercourse between men.

AIG1 affects in vitro and in vivo virulence in clinical isolates of Entamoeba histolytica.

The disease state of amebiasis, caused by Entamoeba histolytica, varies from asymptomatic to severe manifestations that include dysentery and extraintestinal abscesses. The virulence factors of the pathogen, and host defense mechanisms, contribute to the outcomes of infection; however, the underlying genetic factors, which affect clinical outcomes, remain to be fully elucidated. To identify these genetic factors in E. histolytica, we used Illumina next-generation sequencing to conduct a comparative genomic analysis of two clinical isolates obtained from diarrheal and asymptomatic patients (strains KU50 and KU27, respectively). By mapping KU50 and KU27 reads to the genome of a reference HM-1:IMSS strain, we identified two genes (EHI_089440 and EHI_176590) that were absent in strain KU27. In KU27, a single AIG1 (avrRpt2-induced gene 1) family gene (EHI_176590) was found to be deleted, from a tandem array of three AIG1 genes, by homologous recombination between the two flanking genes. Overexpression of the EHI_176590 gene, in strain HM-1:IMSS cl6, resulted in increased formation of cell-surface protrusions and enhanced adhesion to human erythrocytes. The EHI_176590 gene was detected by PCR in 56% of stool samples from symptomatic patients infected with E. histolytica, but only in 15% of stool samples from asymptomatic individuals. This suggests that the presence of the EHI_176590 gene is correlated with the outcomes of infection. Taken together, these data strongly indicate that the AIG1 family protein plays a pivotal role in E. histolytica virulence via regulation of host cell adhesion. Our in-vivo experiments, using a hamster liver abscess model, showed that overexpression or gene silencing of EHI_176590 reduced and increased liver abscess formation, respectively. This suggests that the AIG1 genes may have contrasting roles in virulence depending on the genetic background of the parasite and host environment.

Differential expression of pathogenic genes of Entamoeba histolytica vs E. dispar in a model of infection using human liver tissue explants.

We sought to establish an ex vivo model for examining the interaction of E. histolytica with human tissue, using precision-cut liver slices (PCLS) from donated organs. E. histolytica- or E. dispar-infected PCLS were analyzed at different post-infection times (0, 1, 3, 24 and 48 h) to evaluate the relation between tissue damage and the expression of genes associated with three factors: a) parasite survival (peroxiredoxin, superoxide dismutase and 70 kDa heat shock protein), b) parasite virulence (EhGal/GalNAc lectin, amoebapore, cysteine proteases and calreticulin), and c) the host inflammatory response (various cytokines). Unlike E. dispar (non-pathogenic), E. histolytica produced some damage to the structure of hepatic parenchyma. Overall, greater expression of virulence genes existed in E. histolytica-infected versus E. dispar-infected tissue. Accordingly, there was an increased expression of EhGal/GalNAc lectin, Ehap-a and Ehcp-5, Ehcp-2, ehcp-1 genes with E. histolytica, and a decreased or lack of expression of Ehcp-2, and Ehap-a genes with E. dispar. E. histolytica-infected tissue also exhibited an elevated expression of genes linked to survival, principally peroxiredoxin, superoxide dismutase and Ehhsp-70. Moreover, E. histolytica-infected tissue showed an overexpression of some genes encoding for pro-inflammatory interleukins (ILs), such as il-8, ifn-γ and tnf-α. Contrarily, E. dispar-infected tissue displayed higher levels of il-10, the gene for the corresponding anti-inflammatory cytokine. Additionally, other genes were investigated that are important in the host-parasite relationship, including those encoding for the 20 kDa heat shock protein (HSP-20), the AIG-1 protein, and immune dominant variable surface antigen, as well as for proteins apparently involved in mechanisms for the protection of the trophozoites in different environments (e.g., thioredoxin-reductase, oxido-reductase, and 9 hypothetical proteins). Some of the hypothetical proteins evidenced interesting overexpression rates, however we should wait to their characterization. This finding suggest that the present model could be advantageous for exploring the complex interaction between trophozoites and hepatocytes during the development of ALA, particularly in the initial stages of infection.

[Imported hepatic amebiasis in adults: retrospective study of 58 cases]. / Amœbose hépatique importée de l'adulte : étude rétrospective de cinquante-huit observations.

The authors report the results of a retrospective study of patients hospitalized for serologically- confirmed hepatic amebiasis confirmed by serology in four French military hospitals from January 1, 2002, through December 31, 2012. The study included 58 patients (53 men, 5 women) with a median age of 41 years (range: 25-80). Among them, 34 (59%) were in the military, 10 (17%) were tourists, 10 migrants (15%), and 4 expatriates (5%). For 75%, contamination occurred in sub-Saharan Africa. The qualitative latex test was simple to use and reliable, even in the emergency department. Medical treatment by metronidazole alone was efficacious in 75% of the patients. Indications for drainage must be discussed according to the clinical and laboratory evidence.

[Ultrasonographic features of liver abscess based on a 58-case series in Cameroon]. / Aspects échographiques d'une série de 58 abcès hépatiques au Cameroun.

Amoebic abscess is the most frequent type of liver abscess in tropical areas, including in immunocompromised patients. Abscesses affect the right lobe in 74% of cases and are solitary in more than 80%. The ultrasonographic features of liver abscess vary according to stage, viscosity of liquid contents, amount of debris inside and presence of gas bubbles. Multiple small abcesses are mainly associated with pyogenic abscess and are promoted by HIV infection.

The antiretroviral lectin cyanovirin-N targets well-known and novel targets on the surface of Entamoeba histolytica trophozoites.

Entamoeba histolytica, the protist that causes amebic dysentery and liver abscess, has a truncated Asn-linked glycan (N-glycan) precursor composed of seven sugars (Man(5)GlcNAc(2)). Here, we show that glycoproteins with unmodified N-glycans are aggregated and capped on the surface of E. histolytica trophozoites by the antiretroviral lectin cyanovirin-N and then replenished from large intracellular pools. Cyanovirin-N cocaps the Gal/GalNAc adherence lectin, as well as glycoproteins containing O-phosphodiester-linked glycans recognized by an anti-proteophosphoglycan monoclonal antibody. Cyanovirin-N inhibits phagocytosis by E. histolytica trophozoites of mucin-coated beads, a surrogate assay for amebic virulence. For technical reasons, we used the plant lectin concanavalin A rather than cyanovirin-N to enrich secreted and membrane proteins for mass spectrometric identification. E. histolytica glycoproteins with occupied N-glycan sites include Gal/GalNAc lectins, proteases, and 17 previously hypothetical proteins. The latter glycoproteins, as well as 50 previously hypothetical proteins enriched by concanavalin A, may be vaccine targets as they are abundant and unique. In summary, the antiretroviral lectin cyanovirin-N binds to well-known and novel targets on the surface of E. histolytica that are rapidly replenished from large intracellular pools.

Expression of amoebapores is required for full expression of Entamoeba histolytica virulence in amebic liver abscess but is not necessary for the induction of inflammation or tissue damage in amebic colitis.

Entamoeba histolytica trophozoites produce amoebapores, a family of small amphipathic peptides capable of insertion into bacterial or eukaryotic membranes and causing cellular lysis. Recently, E. histolytica trophozoites that are totally deficient in the production of amoebapore-A were created through a gene silencing mechanism (R. Bracha, Y. Nuchamowitz, and D. Mirelman, Eukaryot. Cell 2:295-305, 2003). Here we tested the virulence of amoebapore A(-) trophozoites in models of the two major forms of amebic disease: amebic liver abscess and amebic colitis. We demonstrate that amoebapore expression is required for full virulence in the SCID mouse model of amebic liver abscess, but E. histolytica trophozoites that do not express amoebapore-A can still cause inflammation and tissue damage in infected human colonic xenografts. These data are consistent with the concept that tissue damage may proceed by different mechanisms in amebic liver abscess compared to amebic colitis.

Alcohol consumption, hepatic iron load and the risk of amoebic liver abscess: a case-control study.

OBJECTIVE: It is unknown why most amoebic liver abscess (ALA) cases occur in alcohol drinkers. In experimental studies, the presence of 'iron' potentiates the in-vitro growth of Entamoeba histolytica (E. histolytica), and is also known to increase its in-vivo invasiveness in animal infections. Chronic alcoholism increases the hepatic iron deposition. We hypothesized that ALA occurs more commonly in livers with a high iron load as in alcoholics. To test this hypothesis we compared the levels of iron between ALA and non-ALA cases belonging to alcoholic and non-alcoholic groups. METHODS: Out of a total of 48 ALA cases, 34 (70%) were alcoholics and 14 (30%) were non-alcoholics. After applying exclusion criteria, serum iron and liver iron stores were quantified in 20 ALA cases (10 alcoholic and 10 non-alcoholics) and compared with 20 non-ALA cases (10 alcoholics and 10 non-alcoholics). RESULTS: All patients of ALA had serum iron values within the normal range but higher than non-ALA cases. In the liver tissue, most patients with ALA had higher (grade II or III) iron deposition, than non-ALA cases (mostly grade I). Thus, patients with ALA, with or without alcohol indulgence, had higher iron levels when compared to the non-ALA cases. CONCLUSION: It appears that the higher incidence of ALA in alcoholic livers is possibly due to their higher iron content.

[Liver abscess and HIV: report of a case]. / Absceso hepático y VIH: a propósito de un caso.

The association of a liver abscess of possible amebic etiology with HIV in a Cuban patient that worked in the Republic of Ethiopia was described. This is important because during the time elapsed since the HIV was described, multiple opportunistic infections were reported, some of them capable of giving rise to the formation of liver abscesses, but none of them with an amebic etiology. In addition, this patient was the first case of liver abscess of possible amebic etiology reported in the whole population of HIV (+) patients studied at "Pedro Kourí" Institute of Tropical Medicine.

Amoebic liver abscess in a patient with human immunodeficiency virus infection.

A thirty two years man, heterosexually promiscuous presented with amoebic liver abscess, proven by ultrasonography, aspiration and culture of organism. He was human immunodeficiency virus (HIV) seropositive and had low CD4+ lymphocyte count. He responded to anti-amoebic treatment.

Blockade of caspases inhibits amebic liver abscess formation in a mouse model of disease.

We looked at the effect of inhibiting caspases on amebic liver abscess in the mouse model of infection. A dose of the pan-caspase inhibitor benzyloxycarbonyl-V-A-D-O-methyl fluoromethyl ketone (Z-VAD-FMK; R & D Systems) given to SCID mice 2 h prior to direct hepatic inoculation with Entamoeba histolytica trophozoites, and 12 h after amebic inoculation, reduced the mean liver abscess size by 70% at 24 h compared to a control group. These data indicate that apoptosis plays a significant but not an exclusive role in amebic liver abscess formation in the mouse model.

Amebic liver abscess.

Amebiasis is a widespread parasitic disease caused by Entamoeba histolytica. This protozoan organism is the third leading parasitic cause of death in the developing world and is an important health risk to travelers in endemic areas. Amebiasis most commonly results in asymptomatic colonization of the gastrointestinal tract, but some patients may develop intestinal invasive disease or extraintestinal disease-amebic liver abscess being the most common extraintestinal manifestation. This article reviews epidemiologic features, pathophysiology, clinical features, diagnostic tests, imaging studies, treatment of amebic liver abscess, and prevention measures.