Fate ofEntamoeba histolyticaduring Establishment of Amoebic Liver Abscess Analyzed by Quantitative Radioimaging and Histology
Autor: | Paulo Tavares, Marie-Christine Rigothier, Ana Cardona, Hout Khun, Michel Huerre, Nancy Guillén |
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Rok vydání: | 2002 |
Předmět: |
Pathology
medicine.medical_specialty Immunology Sulfur Radioisotopes Microbiology Entamoeba histolytica Cricetinae medicine Animals Amoebiasis Abscess Amoebic liver abscess Liver infection biology Dysentery biology.organism_classification medicine.disease Disease Models Animal Infectious Diseases Isotope Labeling Liver Abscess Amebic Radiographic Image Interpretation Computer-Assisted Protozoa Parasitology Fungal and Parasitic Infections Liver abscess |
Zdroj: | Infection and Immunity. 70:3208-3215 |
ISSN: | 1098-5522 0019-9567 |
DOI: | 10.1128/iai.70.6.3208-3215.2002 |
Popis: | The protozoan parasiteEntamoeba histolyticais 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 byE. 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. |
Databáze: | OpenAIRE |
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