Defective production of reactive oxygen intermediates (ROI) in a patient with recurrent amebic liver abscess.

Previously, we reported the case of a man in the fourth decade of life afflicted with three independent episodes of amebic liver abscesses over a period of 4 years. Previous evidence has indicated that the cellular immune response is involved in protection against recurrent invasive amebic infection, and macrophage-mediated effector mechanisms appear important for host resistance to Entamoeba histolytica infection. The aim of the present work was to investigate locomotor activity and oxidative burst function of peripheral mononuclear cells of this individual after healing of the third amebic liver abscess. A locomotion assay using Boyden chemotaxis chambers and the respiratory burst evaluated by chemiluminescence were performed in both mononuclear phagocytes (MPs) and polymorphonuclear (PMN) leukocytes. Levels of salivary IgA and serum IgG anti-amebic antibodies were followed during 48 months after the second amebic liver abscess. Results obtained showed a deficiency in MP but not in PMN leukocyte respiratory burst. Respiratory burst is a major microbicidal mechanism in MP leukocytes; this also has been considered as a host resistance strategy against E. histolytica. It may be at least one risk factor in our patient that was responsible for recurrence of amebic liver abscess.