Immunology of Leishmaniasis and American Trypanosomiasis (Chagas’ Disease)

Abstract

These two important protozoan diseases, leishmaniasis and Chagas’ disease, will be considered together not only because both are caused by species of hemoflagellates that develop intracellularly, but also because the manifestations of both depend to a great extent on the immunological reactions of the host. This is particularly true of the leishmaniases, a group of diseases caused by various species and subspecies of the genus Leishmania all transmitted by sand flies of the genera Phlebotomus, Lutzomyia, and others. All are zoonoses in the sense that a variety of mammals, wild or domesticated, such as rodents, opossums, or dogs, serve as reservoir hosts. As already discussed (Chapter 3), the most remarkable characteristic of the Leishmania is that their habitat in the vertebrate host is within the macrophage, the very cell that normally constitutes the first line of defense against invading organisms. Furthermore, they actually multiply within the phagolysosomes. Somehow they are impervious to the low pH (around 5) and the powerful hydrolases of the phagolysosomal vacuole. Indeed, they have on their surface at least one powerful hydrolase of their own, an acid phosphatase. This enzyme has been found to inhibit superoxide anion production by human neutrophils activated with the chemoattractant peptide f-Met-Leu-Phe. The phosphatase apparently acts on the receptor for the formylated peptide activator. One leishmania contains enough acid phosphatase to reduce by 50% the superoxide anion production of three neutrophils. Since the enzyme has the same effect on macrophages, this may help to explain the reduced respiratory bursts elicited by amastigotes of Leishmania. No doubt other enzymes will be found that help Leishmania to live and grow in the adverse conditions of a phagolysosome.