LEISHMANIA AND HUMAN-IMMUNODEFICIENCY-VIRUS COINFECTION - THE FIRST 10 YEARS

Over 850 Leishmania-human immunodeficiency virus (HN) coinfection case s have been recorded, the majority in Europe, where 7 to 17% of HIV-po sitive individuals with fever have amastigotes, suggesting that Leishm ania-infected individuals without symptoms will express symptoms of le ishmaniasis if they become immunosuppressed. However, there are indire ct reasons and statistical data demonstrating that intravenous drug ad diction plays a specific role in Leishmania infantum transmission: an anthroponotic cycle complementary to the zoonotic one has been suggest ed. Due to anergy in patients with coinfection, L. infantum dermotropi c zymodemes are isolated from patient viscera and a higher L. infantum phenotypic variability is seen. Moreover; insect trypanosomatids that are currently considered nonpathogenic have been isolated from coinfe cted patients. HN infection and Leishmania infection each induce impor tant analogous immunological changes whose effects are multiplied if t hey occur concomitantly, such as a Th1-to-Th2 response switch; however ; the consequences of the viral infection predominate. In fact a large proportion of coinfected patients have no detectable anti-leishmania antibodies. The microorganisms share target cells, and it has been dem onstrated in vitro how L. infantum induces the expression of latent HI V-1. Bone marrow culture is the most useful diagnostic technique, but it is invasive. Blood smears and culture are good alternatives. PCR, x enodiagnosis, and circulating-antigen detection are available only in specialized laboratories. The relationship with low levels of CD4+ cel ls conditions the clinical presentation and evolution of disease. Most patients have visceral leishmaniasis, but asymptomatic, cutaneous, mu cocutaneous, diffuse cutaneous, and post-kala-azar dermal leishmaniasi s can be produced by L. infantum. The digestive and respiratory tracts are frequently parasitized. The course of coinfection is marked by a high relapse rate. There is a lack of randomized prospective treatment trials; therefore, coinfected patients are treated by conventional re gimens. Prophylactic therapy is suggested to be helpful in preventing relapses.