Visceral leishmaniasis in a patient with AIDS: early pathological diagnosis using conventional histology, PCR and electron microscopy is the key for adequate treatment

Leishmaniasis is a disease caused by protozoa that are transmitted by female sand flies (Phlebotomus) from either animals to humans (zoonosis) or from humans to humans (anthroponosis). Currently, approximately 30 sand fly species and 21 different Leishmania species are known, which reside as promastigotes in the gut of the arthropod. Once being inoculated via the skin and internalized in host macrophages and dendritic cells, the promastigotes transform to amastigotes and eventually disseminate via the lymph and blood system [1]. With respect to the organ primarily affected, leishmaniasis comprises four different syndromes: cutaneous leishmaniasis, mucocutaneous leishmaniasis, visceral leishmaniasis (VL; kalar-azar: Hindi for ‘black fever’) and a cutaneous form, which may occur after visceral leishmaniasis (post-kala-azar leishmaniasis—PKDL) [1]. Due to its systemic manifestations, visceral leishmaniasis is a potentially fatal disease with approximately 50,000 deaths per year and an estimated incidence of approx. 500,000/year. This mortality rate in parasitic diseases is second after malaria [2]. After 2–6 months of incubation, VL shows a panel of symptoms including fever, chills, fatigue, weight loss and tiredness. These symptoms are accompanied by hepatoand splenomegaly and sometimes lymphadenopathy and anaemia. However, as our case shows, immunocompromised patients may not present with the full picture of symptoms and manifestations may be atypically localized [2, 3].