Chronic inflammatory disease of skin, mucous membranes or viscera caused by obligate intracellular Kinetoplastid protozoal parasites (Leishmania species) transmitted through infected sand fly. Leishmanial infections like with other intracellular organism (including mycobactria, histoplasma, toxoplasma and tryprosoma) is exacerbated by AIDS.
Different leishmanial parasites in new and old world appeared to show tropism related to temperature, because parasites that cause visceral disease grow at 37% in vitro whereas parasite that cause multiple diseases grow only at 340c. Leishmania are phagocytozed by macrophage and acidity within phagolysosome induces them to transform into amastigate from promatigate by losing flagella. Leismanial amastigotes are the only protozoal parasites that survive and reproduce in macrophage phagolysosomes, which have a PH of 4.5. Amastigotes are protected from the intravascular acid by a proton -transforming ATPase which maintains the intracellular parasite PH at 6.5
Leismanial parasites have two glycocongugates, which appeared important in their virulence. The first is lipophosphoglycans that are glycolipids and bind C3b and iC3b. Organisms resist lysis by complement C5-9 but are phagocytozed by macrophages through complement receptors CR1 and CR3. Lipophosphoglycans may also protect the parasite within phagolysosomes by supplying oxygen radical and by inhibiting lysosmal enzymes. Like M. laprae severity of disease is determined by host immune response.
Visceral leishmaniasis (L.donovanni&L.chagasi) macrophages of RES are invaded so hepatosplenomegly, lymphadenopathy, pancytopenia, fever and weight loss, hyperpigmentation of the skin (kalazar, black fever) glomerulonephritis (mesangioproliferative) and in advanced cases amyloid deposits.
Localized single ulcer on exposed skin (slowly expanding and irregular borders, usually heals within 6 months by involution. The lesion is granulomatous.
Diffuse cutaneous leishmaniasis
Lesions of diffuse cutaneous leishmaniasis resembles lepromatous leprosy nodules. The lesions do not ulcerate but contain vast aggregates of foamy macrophages filled with leishmania. The patients are usually anergic not only to Leshmania but also to other skin antigens and the disease respond poorly to therapy.