The clinical and immunological spectrum of American cutaneous leishmaniasis

Abstract

American cutaneous leishmaniasis is characterized by a spectrum of clinical manifestations. These include localized, often self-healing single lesions, intermediate forms which frequently produce mucosal lesions and often show exaggerated delayed-type hypersensitivity (DTH), and the rare diffuse cutaneous leishmaniasis in which no reaction of protective cell-mediated immunity or DTH can be demonstrated. Clinical, pathological and immunological studies have begun to unravel some of the mechanisms associated with different disease manifestations, dependent on complex interactions between the host immune response, measured in terms of indices including lymphocyte subsets and lymphokines in vitro and within active lesions, and different species of Leishmania.

Phase 1 Study of an Inactivated Vaccine against American Tegumentary Leishmaniasis in Normal Volunteers in Brazil

“…The choice of the Montenegro skin test as a method for evaluating the cellular immune response to LEISHVACINâ was based on characteristics of this response in individuals with ATL, as the presence of a developed and lasting cellular response in cured patients (with and without treatment), and a weak one (anergia) in individuals that are resistant to treatment (Salles Gomes 1939, Manson-Bahr 1987, Convit et al 1993. The Montenegro test is considered highly specific and is used routinely in diagnosing the disease, although it is associated with recent and past infections with Leishmania, and some authors believe it can remain positive throughout the individual's lifetime (Montenegro 1926, Manson-Bahr 1987, Nascimento et al 1993.…”

“…Despite such drawbacks, the Montenegro skin test is considered the safest method for evaluating the immune response to Leishmania infection (Alimohammadian et al 1993, Convit et al 1993, Zijlstra & El-Hassan 1993. However, there is no doubt that a reassessment is required concerning its actual specificity when applied in populations from endemic areas for ATL, the correlation with the in vitro cellular immune response, alteration of the individual's initial response in different areas after one or more tests, and other aspects.…”

Kinetoplastid membrane protein-11 exacerbates infection with Leishmania amazonensis in murine macrophages

“…L. amazonensis infection leads to a spectrum of clinical presentations ranging from a single cutaneous lesion to diffuse cutaneous leishmaniasis, a clinical form that is usually refractory to treatment and is associated with the absence of Leishmania-antigen-specific cell-mediated immune responses (Convit et al 1993). There is evidence that L. amazonensis is able to suppress the potentially effective immune responses of the host (Silveira et al 2004) and that interleukin (IL)-10 contributes, at least in part, to the compromised parasite-specific immunity in L. amazonensisinfected hosts (Jones et al 2002, Ji et al 2003.…”

Las células de Langerhans en la inmunidad a leishmaniasis.

“…A diferencia de lo observado en la leishmaniasis murina experimental, en la leishmaniasis humana la respuesta no es polarizada y se observa, en cambio, un patrón con presencia de citocinas tanto Th1 como Th2, donde el predominio de citocinas propias del perfil Th2 se correlaciona con la persistencia del parásito y con la progresión de la enfermedad, mientras que el control efectivo de la infección y, por tanto,la presentación clínica menos grave ocurre cuando hay predominio de citocinas propias del perfil Th1 que tienen como función principal la activación del macrófago y la subsiguiente muerte del parásito en el interior de su célula hospedera (20)(21)(22)(23)(24).…”