This report describes infection of Drosophila by Leishmania species, a genus of intracellular protozoan parasites that causes disease (leishmaniasis) in humans. It is commonly spread in tropical and subtropical regions by blood-feeding flies in the Phlebotominae genus (Diptera order), often called sand flies.
Wild-type Drosophila injected with L. amazonensis amastigotes derived from mouse macrophages have a roughly 75% survival rate. Mutants in the Toll pathway (Dif) and Imd pathway (PGRP-LC) fare similarly to wild-type flies, as do mutants with melanization defects (Sp7), indicating that those pathways are not a major factor in Drosophila's survival. Unlike in vertebrates (see below), L. amazonensis remain as amastigotes in small vacuoles inside plasmatocytes (hemocyte-derived phagocytic cells).
In flies where CD36-like receptors (CG10345, CG31741, and crq) were knocked down, however, each fly had a greater number of L. amazonensis, and more of them had progressed to the promastigotes phase of their life cycle.
[updated Jan. 2020 by FlyBase; FBrf0222196]
The most common form is cutaneous leishmaniasis, which causes skin sores. The sores typically develop within a few weeks or months of the sand fly bite. The sores may start out as papules (bumps) or nodules (lumps) and may end up as ulcers (like a volcano, with a raised edge and central crater); skin ulcers might be covered by scab or crust. If the sores spread to mucous membranes of the nose, mouth, or throat, it is known as mucosal leishmaniasis. The other main form is visceral leishmaniasis, which affects several internal organs (usually spleen, liver, and bone marrow) and can be life threatening. The illness typically develops within months (sometimes as long as years) of the sand fly bite. Affected people usually have fever, weight loss, enlargement (swelling) of the spleen and liver, and low blood counts - a low red blood cell count (anemia), a low white blood cell count (leukopenia), and a low platelet count (thrombocytopenia). (Adapted from https://www.cdc.gov/parasites/leishmaniasis/disease.html, accessed 2020.01.27.)
Human infection is caused by more than 20 species of Leishmania protozoa. (https://www.cdc.gov/parasites/leishmaniasis/biology.html, accessed 2020.01.27.)
In vertebrates, neutrophils respond to bite sites and phagocytose Leishmania. These neutrophils begin to die and thus display apoptotic markers, causing them to be phagocytosed by dendritic cells and macrophages. Following receptor mediated phagocytosis, the Leishmania-containing phagosome rapidly matures into a phagolysosome-like organelle known as a parasitophorous vacuole, which can contain multiple Leishmania amastigotes (a stage of their life cycle). This vacuole matures in a manner similar to phagolysosome maturation, where it gains markers of early endosomes, late endosomes, and lysosomes. Unlike in phagolysosomes, however, the amastigotes are not degraded, and instead enlarge and modify the vacuole to evade the immune system and support their survival. (Adapted from Ribeiro-Gomes et al. 2012, pubmed:22359507, and Okuda et al. 2016, FBrf0232610.)