Basic Pathophysiology

The various forms of Leishmaniasis (cutaneous, visceral, mucocutaneous and post-kala-azar dermal) are caused by more than 20 different species of protozoa belonging to the genus Leishmania. Visceral Leishmaniasis is caused by L. donovani, L. infantum and L. chagasi. Some who are infected remain asymptomatic while others progress to serious illness and death, at risk are those who are immunocompromised or malnourished. The promastigote (flagellated) form of the parasite multiplies in the gut of female sand flies after it has ingested the amastigote form from another person (or animal). The promastigotes, which are injected into a human host while the sand fly is feeding, are phagocytised by macrophages where they return to an amastigote form. The amastigotes multiply within the macrophage’s phagolysosomes, protected from an immune response by the host.

The incubation period within a human host can range from 10 days up to 2 years. In visceral leishmaniasis the parasite is able to multiply without suppression from the host’s immune system leading to complications affecting the spleen, liver, intestinal mucosa, bone marrow and lymph nodes. Hematopoiesis is depressed leading to pancytopenia, prothrombin becomes depleted (leading to bleeding complications when combined with thrombocytopenia), and decreased albumin predisposes the patient to edema. The host’s immune system becomes severely compromised as infection spreads and, if left untreated, most patients will die within 2-3 years often from secondary infections such as tuberculosis, pneumonia or dysentery.

Leishmania life cycle:

diagram from: http://www.sciencephoto.com/media/151986/enlarge#