The development of post-kala-azar dermal leishmaniasis (PKDL) is associated with acquisition of Leishmania reactivity by peripheral blood mononuclearcells (PBMC)

PKDL develops in about 50% of Sudanese patients treated for visceral leishm aniasis (kala-azar). Patients with kala-azar were entered into this study a nd followed for a period of up to 2 years. During follow up 12 patients dev eloped PKDL and eight did not. Proliferative responses and cytokine product ion to Leishmania donovani and control antigens were measured in vitro usin g PBMC isolated at the time of diagnosis of kala-azar, after treatment of v isceral leishmaniasis, during follow up, and at the time of diagnosis of PK DL. Proliferative responses and interferon-gamma (IFN-gamma) production wer e low at diagnosis and increased after treatment of kala-azar in both patie nts who developed (group 1) and those who did not develop PKDL later (group 2). In group 1, development of PKDL was always associated by an increased PBMC response to Leishmania antigen in proliferation and IFN-gamma producti on assays. There were no differences in Leishmania antigen-induced producti on of IL-4, IL-5 and IL-10 between or within the two groups. We have previo usly shown that Leishmania parasites spread to the skin during visceral lei shmaniasis and proposed that PKDL was the result of an immunological attack on parasites, which have survived in the skin despite the drug treatment. The finding that PKDL develops after treatment of kala-azar as Leishmania-r eactive T cells start to circulate in peripheral blood in sufficient number s to be detected in in vitro assays supports this hypothesis.