Abstract
BackgroundCo-infection of leishmaniasis and HIV is increasingly reported. The clinical presentation of leishmaniasis is determined by the host immune response to the parasite; as a consequence, this presentation will be influenced by HIV-induced immunosuppression. As leishmaniasis commonly affects the skin, increasing immunosuppression changes the clinical presentation, such as in post-kala-azar dermal leishmaniasis (PKDL) and cutaneous leishmaniasis (CL); dermal lesions are also commonly reported in visceral leishmaniasis (VL) and HIV co-infection.MethodsWe reviewed the literature with regard to dermal manifestations in leishmaniasis and HIV co-infection, in three clinical syndromes, according to the primary presentation: PKDL, VL, or CL.ResultsA wide variety of descriptions of dermal leishmaniasis in HIV co-infection has been reported. Lesions are commonly described as florid, symmetrical, non-ulcerating, nodular lesions with atypical distribution and numerous parasites. Pre-existing, unrelated dermal lesions may become parasitized. Parasites lose their tropism and no longer exclusively cause VL or CL. PKDL in HIV co-infected patients is more common and more severe and is not restricted to Leishmania donovani. In VL, dermal lesions occur in up to 18% of patients and may present as (severe) localized cutaneous leishmaniasis, disseminated cutaneous leishmaniasis (DL) or diffuse cutaneous leishmaniasis (DCL); there may be an overlap with para-kala-azar dermal leishmaniasis. In CL, dissemination in the skin may occur resembling DL or DCL; subsequent spread to the viscera may follow. Mucosal lesions are commonly found in VL or CL and HIV co-infection. Classical mucocutaneous leishmaniasis is more severe. Immune reconstitution disease (IRD) is uncommon in HIV co-infected patients with leishmaniasis on antiretroviral treatment (ART).ConclusionWith increasing immunosuppression, the clinical syndromes of CL, VL, and PKDL become more severe and may overlap. These syndromes may be best described as VL with disseminated cutaneous lesions (before, during, or after VL) and disseminated cutaneous leishmaniasis with or without visceralization.
Highlights
Leishmaniasis is divided into three syndromes: cutaneous leishmaniasis (CL) is the most common manifestation with 0.7–1.3 million cases annually [1]
Post-kala-azar dermal leishmaniasis (PKDL) may follow visceral leishmaniasis (VL) in up to 60% of cases; it is important because of the presence of parasites in the skin, and patients may act as a human reservoir (Figure 1) [1,3]
Common characteristics of all syndromes are parasite ‘‘tropism’’ resulting in clear delineation between clinical syndromes. This clinical presentation is the result of the interaction between the parasite and the host immune response; understanding of the underlying immunological mechanisms is important in management that may include drug therapy as well as immunomodulation
Summary
Leishmaniasis is divided into three syndromes: cutaneous leishmaniasis (CL) is the most common manifestation with 0.7–1.3 million cases annually [1]. Post-kala-azar dermal leishmaniasis (PKDL) may follow VL in up to 60% of cases; it is important because of the presence of parasites in the skin, and patients may act as a human reservoir (Figure 1) [1,3]. Involvement of the skin is the key clinical characteristic in all manifestations, except in VL, parasites are present in the normal-looking skin As leishmaniasis commonly affects the skin, increasing immunosuppression changes the clinical presentation, such as in post-kala-azar dermal leishmaniasis (PKDL) and cutaneous leishmaniasis (CL); dermal lesions are commonly reported in visceral leishmaniasis (VL) and HIV coinfection
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