Leishmaniasis is a neglected tropical disease and major public health problem that is endemic in 98 countries. It is caused by different species of the protozoan parasite Leishmania
and is transmitted by the bite of its sand fly vector.
In a recent review article in Cellular Immunology,
Olivier Séguin, and Albert Descoteaux, both from the INRS–Institut Armand-Frappier and the Center for Host-Parasite Interactions, Laval, Canada, discuss how the Leishmania
parasite interacts with the immune system of its mammalian host, and how these interactions affect both the parasite and the host.
is a very complex and specialised parasite that possesses the ability to survive and thrive within its human host,” the authors write.
“To survive, Leishmania
uses an arsenal of pathogenicity factors that includes LPG [lipophosphoglycan] and GP63 to modify the phagosome into a parasitophorous vacuole, modulate the expression and secretion of cytokines, modulate the immune cells flux to the infection site and modulate the antigen presentation favouring a Th2 inefficient response.”
This parasite has a complex life cycle involving two distinct stages: the promastigote form in the female sand fly vector and the amastigote form in the mammalian host.
Leishmania In the Sand Fly
promastigotes multiply and become infectious in the midgut of the sand fly. The infectious promastigotes then migrate to the sand fly esophagus before being inoculated into the mammalian host. When the sand fly bites the mammalian host, the parasites are transferred into the bite wound and are taken up by the host’s inflammatory cells.
Some parasite mortality within the gut of infected sand flies is essential for establishment of infection in the mammalian host. After death, these parasites display the lipid phosphatidylserine (PS) on their surface, a mechanism which allows them to aid survival of the live parasites in the host. This is because the PS tag on the dead parasites dampens down the host’s immune response to the live parasites.