Abstract
Leishmaniasis remains a public health concern around the world that primarily affects poor folks of the developing world spanning across 98 countries with mortality of 0.2 million to 0.4 million annually. Post kala-azar dermal leishmaniasis (PKDL) is the late skin manifestation of visceral leishmaniasis (VL). It has been reported that about 2.5% to 20% of patients recovered from VL develop PKDL having stilted macular or nodular lesions with parasites. In the Indian subcontinent (ISC), it manifests a few months after recovery from VL, though in Africa it can occur simultaneously with VL or a little later. New cases of PKDL are also observed without prior VL in the ISC. These individuals with PKDL represent an important but largely neglected reservoir of infection that perpetuates anthroponotic Leishmania donovani transmission in the ISC and can jeopardize the VL elimination program as these cases can infect the sand flies and spread the endemic. Therefore, it becomes imperative to eradicate PKDL as a part of the VL elimination program. With the limited treatment options besides little knowledge on PKDL, this review stands out in focusing on different aspects that should be dealt for sustained VL elimination.
Highlights
Leishmaniasis or kala-azar, a protozoan parasitic human disease caused by Leishmania parasite in the tropical and subtropical regions through the bite of sand fly (Phlebotomus spp)
Based on its clinical manifestations, this disease occurs into self-healing cutaneous leishmaniasis (CL), skin mucosal ulcers forming mucocutaneous leishmaniasis (MCL), and fatal visceral leishmaniasis (VL), which may be followed by a dermal sequel called Post kala-azar dermal leishmaniasis (PKDL)
The qualitative and quantitative aspects of the parasite in the liver and spleen, where the Leishmania resides, influence the host immunity [63]. These are challenged by the PKDL infection despite systemic protective immunity acquirement known through the cytokine levels and T-cell responses in whole blood or peripheral blood mononuclear cells [64, 65], and organ-specific failure of the memory cell in the skin leads to susceptibility
Summary
Editor: Claudia Ida Brodskyn, Centro de Pesquisa Goncalo Moniz-FIOCRUZ/BA, BRAZIL. The funders had no role in the design, decision to publish, or preparation of the report
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