Fatal visceral disease caused by a dermotropic Leishmania in a patient with human immunodeficiency virus infection

“…Thus, the zymodeme MON-24 is dermotropic and widely distributed throughout the Mediterranean area, having been described in Italy (36), Algeria (29), and Tunisia (117); MON-29 was isolated from cutaneous lesions in southwestern France (208,232,246) and Spain (114); MON-33 was also found in patients from these two countries (208,232); and MON-78 was isolated in Malta (114). These four zymodemes have been isolated from the bone marrow of coinfected patients (48,113,121,122,140,176,232,233,254). The anergic state of HIV-positive subjects permits parasite dissemination, regardless of the isolate's zymodeme (11,140).…”

Section: Visceral Localization Of Cutaneous Zymodemesmentioning

confidence: 99%

Leishmania and human immunodeficiency virus coinfection: the first 10 years

et al. 1997

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Over 850 Leishmania-human immunodeficiency virus (HIV) coinfection cases have been recorded, the majority in Europe, where 7 to 17% of HIV-positive individuals with fever have amastigotes, suggesting that Leishmania-infected individuals without symptoms will express symptoms of leishmaniasis if they become immunosuppressed. However, there are indirect reasons and statistical data demonstrating that intravenous drug addiction plays a specific role in Leishmania infantum transmission: an anthroponotic cycle complementary to the zoonotic one has been suggested. Due to anergy in patients with coinfection, L. infantum dermotropic 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 coinfected patients. HIV infection and Leishmania infection each induce important analogous immunological changes whose effects are multiplied if they 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 demonstrated in vitro how L. infantum induces the expression of latent HIV-1. Bone marrow culture is the most useful diagnostic technique, but it is invasive. Blood smears and culture are good alternatives. PCR, xenodiagnosis, and circulating-antigen detection are available only in specialized laboratories. The relationship with low levels of CD4+ cells conditions the clinical presentation and evolution of disease. Most patients have visceral leishmaniasis, but asymptomatic, cutaneous, mucocutaneous, diffuse cutaneous, and post-kala-azar dermal leishmaniasis 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 regimens. Prophylactic therapy is suggested to be helpful in preventing relapses.

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“…Nevertheless, a number of observations document that virulent Leishmania parasites persist in tissues of cured hosts (reviewed in [2]). In humans, situations of immunosuppression caused either by drug treatment or by infection with HIV may result in reactivation of leishmaniasis [3,4]. In experimental leishmaniasis, live parasites could be recovered from immune mice of strains that are [I 136401 genetically resistant against infection with L. major, the cause of human cutaneous leishmaniasis in the Old World .…”

Section: Introductionmentioning

confidence: 99%

Dendritic cells in Leishmania major‐immune mice harbor persistent parasites and mediate an antigen‐specific T cell immune response

1995

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Upon infection with Leishmania major, a cause of human cutaneous leishmaniasis, mice of resistant strains are able to control the infection, with lesions resolving spontaneously. A long-lasting cell-mediated immunity protects them from reinfection. Nevertheless, small numbers of viable parasites persist in the lymph nodes of these mice. We have recently documented that, in addition to macrophages, epidermal Langerhans cells can ingest L. major. Furthermore, Langerhans cells have the unique ability to transport viable parasites from the infected skin to the draining lymph node for presentation to antigen-specific T cells and initiation of the cellular immune response. During migration, Langerhans cells develop into dendritic cells. In the present study, we analyzed whether dendritic cells support the persistence of parasites in immune hosts. Immunohistological studies and assays in vitro showed that in the lymph nodes of mice that have recovered from infection with L. major, both macrophages and dendritic cells harbor viable parasites. However, only dendritic cells were able to induce a vigorous T-cell immune response to L. major in vitro in the absence of exogenous antigen. Tracking experiments conducted in vivo suggested that the infected dendritic cells in the lymph nodes are derived from Langerhans cells that have emigrated from the skin. The data demonstrate that L. major-infected dendritic cells and macrophages in lymph nodes of immune animals represent long-term host cells, but only dendritic cells have the ability to present endogenous parasite antigen to T cells. Long-term infected dendritic cells may thus allow the sustained stimulation of a population of parasite-specific T cells, protecting the mice from reinfection. Our results favor the hypothesis that the persistence of antigen supports the maintenance of T cell memory and that dendritic cells are critically involved in this process.

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Fatal visceral disease caused by a dermotropic Leishmania in a patient with human immunodeficiency virus infection

Cited by 22 publications

References 7 publications

Response to Heterologous Leishmanins in Cutaneous Leishmaniasis in Nigeria: Discovery of a New Focus

Response to Heterologous Leishmanins in Cutaneous Leishmaniasis in Nigeria: Discovery of a New Focus

Leishmania and human immunodeficiency virus coinfection: the first 10 years

Dendritic cells in Leishmania major‐immune mice harbor persistent parasites and mediate an antigen‐specific T cell immune response

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