Case Study of a Patient With Hiv-Aids and Visceral Leishmaniasis Co-Infection in Multiple Episodes

Abstract

SUMMARYReport of a 45-year-old male farmer, a resident in the forest zone of Pernambuco, who was diagnosed with human immunodeficiency virus (HIV) in 1999 and treated using antiretroviral (ARV) drugs. In 2005, the first episode of visceral leishmaniasis (VL), as assessed by parasitological diagnosis of bone marrow aspirate, was recorded. When admitted to the hospital, the patient presented fever, hepatosplenomegaly, weight loss, and diarrhea. Since then, six additional episodes of VL occurred, with a frequency rate of one per year (2005-2012, except in 2008). In 2011, the patient presented a disseminated skin lesion caused by the amastigotes of Leishmania, as identified by histopathological assessment of skin biopsy samples. In 2005, he was treated with N-methyl-glucamine-antimony and amphotericin B deoxycholate. However, since 2006 because of a reported toxicity, the drug of choice was liposomal amphotericin B. As recommended by the Ministry of Health, this report emphasizes the need for HIV patients living in VL endemic areas to include this parasitosis in their follow-up protocol, particularly after the first infection of VL.

Higher levels of TNF and IL‐4 cytokines and low miR‐182 expression in visceral leishmaniasis‐HIV co‐infected patients

“…This may also explain the greater viral load and lower CD4+ T‐lymphocyte count into this group. However, hitherto published case reports and cross‐sectional studies have not reported a CD4+ T‐lymphocyte count that could be associated with VL‐HIV co‐infection in Brazil . It is therefore difficult to find consensus in studies of the VL‐HIV population, in view of the complex spectrum of clinical and laboratory features.…”

PKDL and Other Dermal Lesions in HIV Co-infected Patients with Leishmaniasis: Review of Clinical Presentation in Relation to Immune Responses

“…This makes clinical suspicion difficult as the clinical presentation of advanced HIV/AIDS and VL (including the effect of medication used) may overlap (splenomegaly, lymphadenopathy, pancytopenia, etc.). In contrast to immunocompetent patients, skin manifestations are not uncommon and may precede or predict recurrence [59] , [61] . In HIV-VL patients, skin lesions confirmed as caused by leishmaniasis were reported in 9%–18% and oral lesions in 3% [62] , [63] .…”

“…In one report, a patient developed DCL 13 months after VL treatment. In another case from Brazil, a papular rash developed after multiple VL episodes with another subsequent VL episode; intercurrent CL was considered as a possibility, as typing was not done [58] , [59] . PKDL in co-infected patients is not restricted to L. donovani because cases of L. infantum/L.…”