A Challenging Case of Visceral Leishmaniasis

The term leishmaniasis includes multiple clinical syndromes: visceral, cutaneous, and mucosal leishmaniasis, resulting from an infection of macrophages throughout the reticuloendothelial system in dermis naso-oropharyngeal mucosa, respectively. phenotype is mainly driven by leishmania biologic characteristics and, ultimately, also host immune status. disease endemic focal areas tropics, subtropics, southern Europe, transmitted bite female phlebotomine sandflies. Sandflies regurgitate parasite’s flagellated promastigote stage into host’s skin; promastigotes bind to receptors on are phagocytized transformed within phagolysosomes non-flagellated amastigotes which replicate infect additional macrophages. Amastigotes ingested sandflies transform back infective promastigotes. Depending innate acquired status, systemic visceral can be characterized irregular fever, weight loss, enlargement spleen liver, anaemia. We present a 42 year-old man with long-lasting type 1 autoimmune hepatitis under immunosuppressive treatment. In January 2017, patient started experience low-grade unresponsiveness empiric antibiotic therapy. developed severe anemia progressive multilineage cytopenia accompanied increased levels inflammatory markers. FDG-PET revealed glucose uptake spleen, whole bone marrow. subsequently performed marrow biopsy evidenced Leishmania inside macrophages, confirmed serological positivity anti-Leishmania antibody. Immunosuppressive therapy was suspended replaced treatment amphotericin B at 4 mg/kg/day day 5, followed single infusion days 10, 17, 24, 31, 38. smear after still few amastigotes; consideration patient’s immunosuppression two further doses 45 52 were employed, leading resolution. real-life, as exemplified this case, administering (concerning guidelines) offered therapeutic opportunity for long-term