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Review
. 2016 Aug 23;9(1):464.
doi: 10.1186/s13071-016-1721-0.

The immunology of post-kala-azar dermal leishmaniasis (PKDL)

Eduard E Zijlstra  1
Affiliations
Review

The immunology of post-kala-azar dermal leishmaniasis (PKDL)

Eduard E Zijlstra. Parasit Vectors. .

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.

Keywords: Clinical features; Immune manipulation; Immune responses; Immunosuppression; PKDL; Post-kala-azar dermal leishmaniasis; Visceral leishmaniasis.

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Figures

Fig. 1
Fig. 1
Typical PKDL from Sudan with papular lesions. ©World Health Organization, 2012. Reproduced unmodified from reference [77]
Fig. 2
Fig. 2
Typical PKDL from Bangladesh with (confluent) macular rash. ©World Health Organization, 2012. Reproduced unmodified from reference [77]
Fig. 3
Fig. 3
Schematic representation of clinical presentation, corresponding immune responses and areas of missing information using the Th1/Th2 dichotomy. *Most important parameters that determine the immunologically relevant response. a, b the intervals differ in time between regions: 0–13 months in Africa; 0–3 years in Asia. There is limited information on (the timing of) the developing or changing immune response in relation to type of VL treatment (or in case of absent VL history) and the clinical response (macular, papular, nodular PKDL; distribution and severity). c the interval after successful treatment of VL and establishment of permanent immunity is unknown. d, e there is no information on (the timing of) the developing or changing immune response (after PKDL treatment or after self-healing), the clinical response (reduction or disappearance of lesions) and development of immunity
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