Post-kala-azar dermal leishmaniasis (PKDL) is a cutaneous manifestation of visceral leishmaniasis (VL), characterized by skin lesions, nodules or papules, frequently on the face. It often appears 2-7 years after the apparently successful treatment of VL by antimonial drugs. It has long been considered a curious phenomenon, difficult to treat and difficult to explain. Recent studies have sought to determine parasite, host and treatment factors that might explain the cause(s) of PKDL. First, is there anything special about the parasite? PKDL is caused by Leishmania donovani in India and Sudan, with a few cases reported to be caused by L. infantum / chagasi and historically by either species in China. Recent molecular studies in India and Sudan on PKDL and VL clinical isolates have not identified or defined any strains characteristically associated with the problem (1-3). It seems unlikely to be a parasite determined manifestation of leishmaniasis. Second, is there anything different about PKDL patients, their immunological status, susceptibility or other factors? Clinical reports have not identified sex, age or racial origin as defining factors (4). A possibility that genetic disposition might be involved was indicated in Sudan where genotypic studies identified linkage of the interferon-[gamma] (IFN-[gamma]) receptor to PKDL and not to VL. But further studies are required to clearly define susceptibility factors. The immunological status of PKDL patients continues to be characterized but the picture is complex with mixed T cell responses and elevated levels of interleukin-10 (IL-10) and tumour necrosis factor alpha (TNF-[alpha]) (6-9).