Abstract
Post-kala-azar dermal leishmaniasis (PKDL) is a common complication of visceral leishmaniasis (VL) caused by Leishmania donovani. Because of its possible role in transmission it is considered a public health problem in VL endemic areas. The clinical features include a skin rash consisting of macules, papules or nodules in an otherwise healthy individual; this presentation is determined by the immune response towards parasites in the skin that probably persisted from the previous VL episode. The immune response in VL, cured VL and PKDL is the result of changes in the cytokine profile that only in part can be captured under the Th1 and Th2 dichotomy. Regulatory T cells and Th 17 cells also play a role. VL is characterized by an absent immune response to Leishmania with a predominantly Th2 type of response with high levels of IL-10; after successful treatment the patient will be immune with in vitro features of a Th1 type of response and in vivo a positive leishmanin skin test. PKDL takes an intermediate position with a dissociation of the immune response between the skin and the viscera, with a Th2 and Th1 type of response, respectively. It is likely that immune responses determine the different epidemiological and clinical characteristics of PKDL in Asia and Africa; various risk factors for PKDL may influence this, such as incomplete and inadequate treatment of VL, parasite resistance and genetic factors. It should be noted that PKDL is a heterogeneous and dynamic condition and patients differ with regard to time of onset after visceral leishmaniasis (VL), chronicity, extent and appearance of the rash including related immune responses, all of which may vary over time. Better understanding of these immune responses may offer opportunities for manipulation including combined chemotherapy and immunotherapy for VL to prevent PKDL from occurring and similarly in the treatment of chronic or treatment resistant PKDL cases.
Highlights
Post-Kala-azar Dermal Leishmaniasis (PKDL) may follow after treatment of visceral leishmaniasis (VL, kala-azar)
In this paper we describe the principal immunological features of Post-kala-azar dermal leishmaniasis (PKDL), in particular in relation to VL, and correlate these findings with clinical and epidemiological knowledge
As typically the PKDL lesions occur in sun exposed areas of the skin, the immune response is thought to be related to the influence of UV light; this causes damage to dendritic cells resulting in a Th2 type of response by inhibition of regulatory T cells. [32, 35,36,37] In PKDL increased levels of IL-10 expressing CD3+CD8+ regulatory cells were found in the skin that decrease after treatment [7]
Summary
Post-Kala-azar Dermal Leishmaniasis (PKDL) may follow after treatment of visceral leishmaniasis (VL, kala-azar). Marker for cure clinical arecent data show that up to 30 % of PKDL in Asia occurs within 12 months after treatment for VL bthis is called para-kala-azar dermal leishmaniasis Before treatment After infection in the skin by the sand fly, the innate immune response includes interaction with neutrophils and complement after which the parasite infects macrophages/monocytes.
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