Visceral Leishmaniasis in Pediatrics: A Case Series and a Narrative Review with Global Insights

Abstract

Visceral leishmaniasis (VL) is a severe parasitic disease caused by Leishmania spp., with a significant impact on pediatric populations, particularly in endemic regions. The diagnosis of VL in children requires a high index of suspicion, as clinical manifestations-such as prolonged fever, hepatosplenomegaly, and pancytopenia-overlap with other infectious and hematologic diseases. While serological and molecular tests aid in detection, bone marrow aspiration remains the gold standard for definitive diagnosis. In this case series, we describe five pediatric patients diagnosed with VL in Italy, emphasizing the importance of a timely and accurate diagnostic approach. Liposomal amphotericin B (LAmB) is the first-line treatment in Southern Europe due to its high efficacy and reduced toxicity. Our patients received a standard regimen of 3 mg/kg daily for five days, plus an additional dose on day 10, leading to rapid clinical improvement. However, some cases required supportive care, such as red blood cell transfusions, particularly in patients with co-infections. Despite being a neglected disease, VL is re-emerging in Europe, influenced by climate change, increased pet ownership, and migration from endemic regions. Prevention strategies focus on vector control, canine vaccination, and public health awareness. The global rise in pediatric VL highlights the need for improved surveillance, access to affordable treatments, and the development of effective vaccines to mitigate the disease burden in both endemic and non-endemic areas.

Keywords: bone marrow aspiration; hemophagocytic lymphohistiocytosis; liposomal amphotericin B; neglected tropical diseases; pediatric emergency department; vector control; visceral leishmaniasis; zoonosis.

Figure 1

Schematic of Leishmania infantum. Life cycle: sandflies transmit promastigotes to humans and animal reservoirs. In the host, promastigotes are phagocytosed by macrophages (A) and differentiate into amastigotes (B). Amastigote replication leads to macrophage lysis (C) and dissemination mainly to reticuloendothelial organs—spleen, liver, and bone marrow (D)—causing VL manifestations.