The cause of<unk>  is uncertain. Possibilities may include use of antimonial drugs, sunburn, reinfection with<unk> -azar, memory T cell responses failing in certain organs; and genetic susceptibility. There is increasing evidence that the pathogenesis is largely immunologically mediated; high concentrations of interleukin 10 in the peripheral blood of VL patients predict the development of<unk> . During VL, interferon gamma is not produced by peripheral blood mononuclear cells (PBMC). After treatment of VL, PBMCs start producing interferon gamma, which coincides with the appearance of<unk>  lesions due to interferon-gamma-producing cells causing skin inflammation as a reaction to persisting parasites in the skin.
Post-kala-azar dermal leishmaniasis
Melanie's Marvelous Measles
Cutaneous leishmaniasis
Granuloma gluteale infantum
Rickettsialpox
Leishmaniasis
Flying squirrel typhus
Progressive vaccinia