Abstract

Visceral leishmaniasis (VL) is a parasitic protozoon infection caused by the Leishmania species and transmitted by sandflies. Patients acquire VL in five main tropical areas and the Mediterranean basin, and clinicians from non-endemic regions regularly see infected patients. We describe the population presenting with VL to the Hospital for Tropical Diseases (HTD), London and identify risk factors for developing VL.Methods and Principal FindingsA retrospective study of imported VL to the HTD, London including patients diagnosed and/or managed at the HTD between January 1995 and July 2013. We analyse patient demographics, risk factors for developing VL, diagnosis, investigation, management and outcome. Twenty-eight patients were treated for VL at the HTD over an 18 year period. The median age at VL diagnosis was 44 years (range 4–87 years) with a male to female ratio of 2:1. Most patients were British and acquired their infection in the Mediterranean basin. The median time from first symptom to diagnosis was six months with a range of 1–12 months and diagnosis included microscopic visualisation of leishmania amastigotes, positive serological tests (DAT and k39 antibody) or identification of leishmania DNA. Nineteen patients had some form of immunocompromise and this has increased proportionally compared to previously described data. Within the immunocompromised group, the ratio of those with autoimmune disease has increased. Immunocompromised patients had lower cure and higher relapse rates.ConclusionsThe rise of VL in patients with immunocompromise secondary to autoimmune disease on immunomodulatory drugs presents new diagnostic and therapeutic challenges. VL should be a differential diagnosis in immunocompromised patients with pyrexia of unknown origin returning from travel in leishmania endemic areas.

Highlights

  • Visceral leishmaniasis (VL) is a parasitic infection caused by the Leishmania species and is transmitted by the sandfly. [1] The annual global incidence of VL is over half a million cases in the endemic zones of Nepal, India, Bangladesh, Sudan, Brazil and the Mediterranean basin [2] With increasing global travel, clinicians from non-endemic regions are encountering more patients with VL infection.[3,4]Patients with VL present with chronic pyrexia, anorexia, splenomegaly and pancytopenia

  • Visceral Leishmaniasis and Immunocompromise be a differential diagnosis in immunocompromised patients with pyrexia of unknown origin returning from travel in leishmania endemic areas

  • We present a retrospective study of imported VL cases diagnosed and/or managed at the Hospital for Tropical Diseases (HTD), London between 1995 and 2013, and identify new risk factors for developing VL

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Summary

Introduction

Visceral leishmaniasis (VL) is a parasitic infection caused by the Leishmania species and is transmitted by the sandfly. [1] The annual global incidence of VL is over half a million cases in the endemic zones of Nepal, India, Bangladesh, Sudan, Brazil and the Mediterranean basin [2] With increasing global travel, clinicians from non-endemic regions are encountering more patients with VL infection.[3,4]Patients with VL present with chronic pyrexia, anorexia, splenomegaly and pancytopenia. Visceral leishmaniasis (VL) is a parasitic infection caused by the Leishmania species and is transmitted by the sandfly. [1] The annual global incidence of VL is over half a million cases in the endemic zones of Nepal, India, Bangladesh, Sudan, Brazil and the Mediterranean basin [2] With increasing global travel, clinicians from non-endemic regions are encountering more patients with VL infection.[3,4]. There is a spectrum of clinical disease that depends upon the interplay between the host immune response and the parasite species and load. Th-1 secrete several cytokines (IL-2, INF gamma and TNF alpha) recruiting and activating macrophages that phagocytose the cells with leishmania amastigotes.[7] In the immunosuppressed patients, T cell responses are inadequate and patients have increased susceptibility to developing clinical disease, experience a more severe disease course and have higher rates of relapse. Whilst risk factors for developing VL in endemic zones are well defined, [11] there is little published evidence of the risk factors for developing VL in a non-endemic setting

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