Post-kala-azar dermal leishmaniasis (PKDL) is a dermatosis that affects more than 50% of successfully treated visceral leishmaniasis (VL) patients in Sudan. PKDL is considered an important reservoir for the parasite and its treatment may help in the control of VL. Currently, treatment is mainly with sodium stibogluconate (SSG), an expensive and fairly toxic drug and without universally in treatment protocols used. A literature review, a consensus of a panel of experts, and unpublished data formed the basis for the development of guidelines for the treatment of PKDL in the Sudan. Six treatment modalities were evaluated. Experts were asked to justify their choices based on their experience regarding of drug safety, efficacy, availability, and cost. The consensus was defined by assigning a categorical rank (first line, second line, third line) to each option. Regarding the use of AmBisome the presence of the drug in the skin was confirmed in smears from PKDL lesions. Recommendations: AmBisome at 2.5？mg/kg/day/20 days or SSG at 20？mg/kg/day/40 days plus four/weekly intradermal injection of alum-precipitated autoclave L. major vaccine are suggested as first- and second-treatment options for PKDL in the Sudan, respectively. SSG at 20？mg/Kg/day/60 or more days can be used if other options are not available. 1. Introduction Post-kala-azar dermal Leishmaniasis (PKDL) is a complication of visceral Leishmaniasis (VL) that emerges as a new disease entity following successful treatment of VL. In few cases PKDL may follow subclinical infection with L donovani. It occurs with a frequency of ~56% of successfully treated VL patients in the Sudan [1–5]. The disease has been described with a lower frequency in India, Nepal, and Bangladesh [6]. In Sudan, the skin lesions heal spontaneously in ~85% of patients, while in 15% of patients lesions persist and require medical treatment [4]. The disease can be very severe affecting the mucous membrane and interfering with feeding in the very young [4]. PKDL lesions (especially nodular forms) are probably an important source of transmission in the Sudan and the Indian subcontinent [7]. In addition, some reports suggested that the incidence of antimony refractoriness in VL patients is due to the anthroponotic transmission of refractory strains from PKDL patients thus increasing the burden of drug resistance [8]. Cytokines, drugs, and Ultraviolet light (UVB) have been suggested as possible factors involved in the pathogenesis of Sudanese PKDL [9–11]. The pathology is well documented. It consists of hyperkeratosis, parakeratosis,
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