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      Leishmaniasis–HIV coinfection: current challenges

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          Abstract

          Leishmaniasis – human immunodeficiency virus (HIV) coinfection can manifest itself as tegumentary or visceral leishmaniasis. Almost 35 countries have reported autochthonous coinfections. Visceral leishmaniasis is more frequently described. However, usual and unusual manifestations of tegumentary leishmaniasis have been reported mainly in the Americas, but the real prevalence of Leishmania infection in HIV-infected patients is not clear. Regarding the clinical manifestations, there are some reports showing unusual manifestations in visceral leishmaniasis and tegumentary leishmaniasis in HIV-infected patients; yet, the usual manifestations are more frequent. Leishmaniasis diagnosis relies on clinical methods, but serological tests are used to diagnose visceral leishmaniasis despite them having a low sensitivity to tegumentary leishmaniasis. The search for the parasite is used to diagnose both visceral leishmaniasis and tegumentary leishmaniasis. Nevertheless, in HIV-infected patients, the sensitivity of serology is very low. Drugs available to treat leishmaniasis are more restricted and cause severe side effects. Furthermore, in HIV-infected patients, these side effects are more prominent and relapses and lethality are more recurrent. In this article, we discuss the current challenges of tegumentary leishmaniasis and visceral leishmaniasis–HIV infection, focusing mainly on the clinical manifestations, diagnosis, and treatment of leishmaniasis.

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          Most cited references 80

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          Control of the leishmaniases.

            (2009)
          This report makes recommendations on new therapeutic regimens for visceral and cutaneous leishmaniasis, on the use of rapid diagnostic tests, details on the management of Leishmania-HIV coinfection and consideration of social factors and climate change as risk factors for increased spread. Recommendations for research include the furtherance of epidemiological knowledge of the disease and clinical studies to address the lack of an evidence-based therapeutic regimen for cutaneous and mucocutaneous leishmaniasis and post-kala-azar dermal leishmaniasis (PKDL). This report not only provides clear guidance on implementation but should also raise awareness about the global burden of leishmaniasis and its neglect. It puts forward directions for formulation of national control programmes and elaborates the strategic approaches in the fight against the leishmaniases. The committee's work reflects the latest scientific and other relevant developments in the field of leishmaniasis that can be considered by member states when setting national programmes and making public health decisions.
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            Current diagnosis and treatment of cutaneous and mucocutaneous leishmaniasis.

            Tegumentary leishmaniasis, comprising the cutaneous and mucocutaneous forms, is caused by at least 13 dermotropic species of protozoa of the genus Leishmania, most of which are prevalent in the New World. Although diseases in the Old and New Worlds share similar characteristics, the ultimate manifestations and severity are quite different, with more severe forms associated with mucosal lesions observed in the New World. For the diagnosis and treatment of leishmaniasis, differences based on clinical features, usefulness/sensitivity of diagnostic methods and therapeutic responses are mainly emphasized. We present a critical review of the diagnostic methods, their contribution and the necessity for their improvement/development, particularly in molecular diagnosis aimed at detection and species identification, as well as serodiagnosis. In addition to a review of the drugs currently utilized, we describe differences in their effectiveness in Old and New World leishmaniasis. HIV/Leishmania coinfection is also presented in the context of diagnosis and treatment.
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              Paradoxical worsening of tuberculosis following antiretroviral therapy in patients with AIDS.

              Transient worsening of tuberculous symptomatology and lesions following antituberculous therapy (paradoxical response) has previously been described as a rare occurrence. To determine the incidence of paradoxical responses in patients with AIDS and TB who are treated with antituberculous therapy and subsequently with combination antiretroviral therapy (ARV), we conducted a prospective study of 33 HIV-seropositive TB patients treated with anti-TB therapy and antiretroviral therapy (Group 1) compared with 55 HIV-seronegative TB patients treated with anti-TB therapy (Group 2) and 28 HIV-seropositive TB patients treated with anti-TB therapy but not on antiretrovirals (historical control; Group 3). In Group 1 patients, paradoxical responses were temporally more related to the initiation of ARV than to the initiation of anti-TB therapy (mean +/- SD: 15 +/- 11 d versus 109 +/- 72 d [p < 0.001]) and occurred much more frequently (12 of 33; 36%) compared with Group 2 (1 of 55; 2%) (p < 0.001) or with Group 3 (2 of 28; 7%) (p = 0.013). The majority of patients who experienced paradoxical responses and received tuberculin purified protein derivative (PPD) in Group 1 had their tuberculin skin tests convert from negative to strongly positive after ARV. These observations suggest that a paradoxical response associated with enhanced tuberculin skin reactivity may occur after the initiation of ARV in HIV-infected TB patients. Furthermore, the skin test conversion after the initiation of ARV may have important public health implications.
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                Author and article information

                Journal
                HIV AIDS (Auckl)
                HIV AIDS (Auckl)
                HIV/AIDS - Research and Palliative Care
                HIV/AIDS (Auckland, N.Z.)
                Dove Medical Press
                1179-1373
                2016
                07 October 2016
                : 8
                : 147-156
                Affiliations
                [1 ]Laboratory of Soroepidemiology (LIM HC-FMUSP), São Paulo University, São Paulo
                [2 ]Instituto de Infectologia Emilio Ribas-SES, São Paulo
                [3 ]Department of Infectious Disease, Faculty of Medicine, São Paulo University, São Paulo
                [4 ]Hospital Giselda Trigueiro - SESAP, Natal, Brazil
                Author notes
                Correspondence: José Angelo Lauletta Lindoso, Laboratório de Soroepidemiologia, Instituto de Medicina Tropical da Universidade de São Paulo and Instituto de Infectologia Emilio Ribas, Avenida Dr Eneas de Carvalho Aguiar, 450, Cerqueira Cézar, 05403000 São Paulo, Brazil, Tel +55 11 3061 7023, Fax +55 11 3061 7028, Email jlindoso@ 123456usp.br
                Article
                hiv-8-147
                10.2147/HIV.S93789
                5063600
                © 2016 Lindoso et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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