Humoral Immune Responses to Amebic Liver Abscess

Background: Amebic liver abscess (ALA) is an ancient parasitic disease caused by E. histolytica described first by Hippocrates. It is endemic worldwide, mainly in tropic and subtropics countries. About 50 million true E. histolytica infections and approximately 100,000 deaths occur each year globally. In Bangladesh, exact incidences of amebic liver abscess cases are not estimated, but hospital reports indicate that it is endemic. Immunity and immune responses in acute and post infections of ALA are not well understood to date. However, the understanding of immunology is essential to know disease progression, recovery, morbidity, and mortality as well as diagnosis and newer prevention strategies like vaccine development. In this 15-month prospective and follow-up study, different antibody responses are estimated periodically. Methods: About 90 amebic liver abscess patients diagnosed initially by ultra-sonogram confirmed followed by Real-Time PCR were selected for this study. All were admitted into Rajshahi Medical College Hospital, Bangladesh. Antibody responses against different antigens, which include Serum anti-lectin IgG, Salivary anti-CRD (carbohydrate recognition domain) Ig A, and Stool anti-CRD (carbohydrate recognition domain) IgA were estimated by ELISA periodically thrice, in acute stage after 06 and 09 months and between 12 and 15 months. Results: Serum anti-lectin IgG in ALA persists remarkably high well up to 09 months in 98% cases, Secretory anti-CRD IgA was also determined from the saliva, and only 36(40%) show positive titer during first 06 months, and about 40% of ALA cases show high titer of anti-CRD IgA from stool samples in first six months of infection. Conclusion: Only serum anti lectin Ig G showed significant high titer in 98% of cases in the acute stage and up to nine months of infection. TAJ 2021; 34: No-1: 05-08

Amebic Liver Abscess

Objective: Amebic liver abscess (ALA) is endemic to many areas of the world. In this study we sought to investigate the epidemiology, presentation, laboratory tests and imaging characteristics related to ALA in Oman and ultimately determine whether ALA is native to Oman or is it imported from abroad. Methods: This case series study was conducted at Royal Hospital Muscat, Oman. Patient data was extracted from the Royal Hospital patient database and included patients older than 13 years of age, discharged with the discharge diagnosis of ALA from January 2013 to December 2017. Results: 22 patients were included in the study. The results showed 18 Omani patients and 4 expatriates. Only two Omanis had history of travel abroad. 15 patients were male and 7 females. The average age was 45.2. The most common presentation was abdominal pain seen in 17 patients. Fever was seen in 13 patients. Alanine transferase was found to be elevated in 13 patients. 90% of patients had no symptomatic infections prior to developing ALA. Conclusion: The data suggests that ALA is endemic to Oman given the higher number of local patients and the lack of travel abroad in this population. As the number of treated ALA patients is rather small, it can be concluded that the occurrence of ALA is much lower in Oman as compared to other endemic areas. The majority of patients had no prior symptomatic infections and thus a method of control would be to screen and prevent amebic spread. Keywords: Amebic liver abscess, Amebiasis, liver abscess, Entamoeba histolytica, Royal Hospital, Oman

Evaluation of the PEΔIII-LC3-KDEL3 Chimeric Protein of Entamoeba histolytica-Lectin as a Vaccine Candidate against Amebic Liver Abscess

Entamoeba histolytica is an intestinal parasite that causes dysentery and amebic liver abscess. E. histolytica has the capability to invade host tissue by union of virulence factor Gal/GalNAc lectin; this molecule induces an adherence-inhibitory antibody response as well as to protect against amebic liver abscess (ALA). The present work showed the effect of the immunization with PEΔIII-LC3-KDEL3 recombinant protein. In vitro, this candidate vaccine inhibited adherence of E. histolytica trophozoites to HepG2 cell monolayer, avoiding the cytolysis, and in a hamster model, we observed a vaccine-induced protection against the damage to tissue liver and the inhibition of uncontrolled inflammation. PEΔIII-LC3-KDEL3 reduced the expression of TNF-α, IL-1β, and NF-κB in all immunized groups at 4- and 7-day postinfection. The levels of IL-10, FOXP3, and IFN-γ were elevated at 7 days. The immunohistochemistry assay confirmed this result, revealing an elevated quantity of +IFN-γ cells in the liver tissue. ALA formation in hamsters immunized was minimal, and few trophozoites were identified. Hence, immunization with PEΔIII-LC3-KDEL3 herein prevented invasive amebiasis, avoided an acute proinflammatory response, and activated a protective response within a short time. Finally, this recombinant protein induced an increase of serum IgG.