Vaccine Efficacy of Leishmania donovani Membrane Antigens Against Experimental Visceral Leishmaniasis

Leishmaniasis is caused by protozoan parasites of the Leishmania species that are transmitted by the bite of phlebotomine sandflies. In vertebrate hosts, Leishmania survive and multiply as non-motile amastigotes, primarily in macrophages. Amastigotes are ingested when a female sandfly takes a blood meal from an infected host. In the sandfly, amastigotes undergo a developmental programme culminating in the generation of infective metacyclic, flagellated promastigotes, which are introduced into the skin with the sandfly saliva at the next blood meal. Leishmaniasis has been traditionally classified into three major clinical entities: cutaneous, mucocutaneous and visceral. Cutaneous leishmaniasis results in formation of skin ulcers at the site of the sandfly bite, usually on exposed parts of the body, the face, neck, arms and legs. In mucocutaneous leishmaniasis, the initial skin lesions cure, but the late development of metastatic lesions can lead to partial or total destruction of the mucous membranes. Visceral leishmaniasis, also known as kala-azar, is the most severe and often fatal syndrome. It results in the pentad of syndromes comprised of fever, weight loss, splenomegaly, hepatomegaly and anaemia. If left untreated, the disease has a high mortality rate mainly due to immunosuppression and secondary infections. Some individuals develop the unusual syndrome known as post kala-azar dermal leishmaniasis (PKDL), which appears within a few years of the complete cure of visceral leishmaniasis. Visceral leishmaniasis has become a frequent infection in HIV positive individuals in nendemic areas