Visceral and cutaneous leishmaniasis recommendations for solid organ transplant recipients and donors

• Autor(a) principal: Wanessa Trindade Clemente
• Data de Publicação: 2017
• Outros Autores: Paulo Henrique Orlandi Mourão, Francisco Lopez-medrano, Brian s. Schwartz, Carmen García-donoso, Julian Torre-cisneros
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFMG
• Texto Completo: http://hdl.handle.net/1843/55705; https://orcid.org/0000-0003-0848-3740
• topic: Cutaneous leishmaniasis; Visceral leishmaniasis; Organ Transplantation; Leishmaniose Tegumentar Difusa; Leishmaniose Visceral; Transplante de orgãos

Leishmaniasis is a protozoan disease transmitted through the bite of infected female sandflies of the genera Phlebotomus (Old World) and Lutzomyia (New World). Infection with Leishmania species may cause cutaneous, mucocutaneous, or visceral leishmaniasis (VL). Cutaneous leishmaniasis (CL) is characterized by single or multiple skin ulcers, satellite lesions, or nodular lymphangitis and is associated with multiple species . Mucocutaneous leishmaniasis (MCL) is often caused by L. braziliensis and L. panamensis, and leads to metastasis of the disease to the mucosal tissues of the mouth and upper respiratory tract via lymphatic or hematogenous dissemination . VL in the New World is caused by L. infantum (= L. chagasi).In this form, the parasite can infect internal organs, such as the liver, spleen, and bone marrow, causing life-threatening diseases. However, in immunocompromised hosts, such as organ transplant recipients, the clinical presentation of this disease and the response to treatment can be greatly altered.Reported cases of leishmaniasis in solid-organ transplant (SOT) recipients have been predominantly VL; CL is rarely reported among these patients.5 It remains unclear whether this difference occurs because SOT leads to a greater susceptibility to VL, because fewer organ transplants are performed in areas highly endemic for CL or because of a publication bias. In a recent study, VL prevalence among SOT recipients ranged from 0.1% to 0.5% in endemic countries. The factors causing infected individuals to develop clinicaldisease are only partially understood; however, parasite virulence, nutritional status, age, and host genetic and response factors are known to contribute to the development of clinical disease.8 Seventy percent of individuals can be asymptomatically infected in highly endemic areas, depending on the geographic location and detection technique used In healthy, immunocompetent hosts, T helper cells kill Leishmania protozoa. However, in immunosuppressed patients, the T-cell response is inadequate, thus increasing the susceptibility of these patients to develop clinical disease or more severe disease and leading to higher rates of relapse. In organ transplant recipients, the risk factors for developing leishmaniasis have been poorly studied. Immunosuppression, especially due to the use of high-dose steroids, may play a role in the development.of disease.11 Leishmaniasis is frequently described in renal transplant recipients. This finding may be attributed to the higher number of renal transplants compared with other organs or to a publication bias; although, it is conceivable that renal failure or dialysis may increase the risk of developing leishmaniasis via an as-yet-unknown mechanism. Transplant patients can develop leishmaniasis by (i)primary infection via a vector, (ii) reactivation of a latent infection, or (iii) donor-derived infection (organ or blood).16,17 Leishmani asis should be suspected in transplant recipients from endemic areas or in those who have traveled to endemic areas, even if they did so many years before transplantation.3 Leishmaniasis can occur at any time after transplantation; although, most infections present in the first year posttransplant.5,11,18 There is evidence linking the intensity of endemicity in an area withearly infection after transplantation.