Zijlstra Eduard E
Rotterdam Centre for Tropical Medicine, Rotterdam, The Netherlands.
PLoS Negl Trop Dis. 2014 Nov 20;8(11):e3258. doi: 10.1371/journal.pntd.0003258. eCollection 2014.
Co-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.
We 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.
A 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).
With 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.
利什曼病与艾滋病毒合并感染的报道日益增多。利什曼病的临床表现取决于宿主对寄生虫的免疫反应；因此，这种表现会受到艾滋病毒诱导的免疫抑制的影响。由于利什曼病通常会影响皮肤，免疫抑制的增加会改变临床表现，如在黑热病后皮肤利什曼病（PKDL）和皮肤利什曼病（CL）中；在内脏利什曼病（VL）和艾滋病毒合并感染中也常见皮肤病变。
我们根据主要表现，对三种临床综合征（PKDL、VL或CL）中利什曼病与艾滋病毒合并感染的皮肤表现相关文献进行了综述。
已有关于艾滋病毒合并感染时皮肤利什曼病的多种描述。病变通常被描述为皮疹明显、对称、非溃疡性、结节性病变，分布不典型且寄生虫众多。先前存在的、无关的皮肤病变可能会被寄生。寄生虫失去其嗜性，不再仅导致VL或CL。艾滋病毒合并感染患者中的PKDL更常见且更严重，并且不限于杜氏利什曼原虫。在VL中，高达18%的患者会出现皮肤病变，可能表现为（严重）局限性皮肤利什曼病、播散性皮肤利什曼病（DL）或弥漫性皮肤利什曼病（DCL）；可能与黑热病后皮肤利什曼病重叠。在CL中，皮肤内可能会出现类似DL或DCL的播散；随后可能会扩散至内脏。粘膜病变在VL或CL与艾滋病毒合并感染中很常见。典型的粘膜皮肤利什曼病更严重。在接受抗逆转录病毒治疗（ART）的艾滋病毒合并感染利什曼病患者中，免疫重建疾病（IRD）并不常见。
随着免疫抑制的增加，CL、VL和PKDL的临床综合征变得更严重，且可能重叠。这些综合征最好描述为伴有播散性皮肤病变的VL（在VL之前、期间或之后）以及伴有或不伴有内脏受累的播散性皮肤利什曼病。
