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Updated: May 6, 2026
In vivo Imaging of Transgenic Leishmania Parasites in a Live Host
Published on: July 27, 2010
Systematic suppression of Leishmania (Leishmania) amazonensis-mediated delayed-type hypersensitivity response in
Marliane B Campos1, Luciana V R Lima1, Thiago Vasconcelos Dos Santos1
1Evandro Chagas Institute (Surveillance Secretary of Health and Environment, Ministry of Health), Ananindeua, Pará, Brazil.
Background:
American cutaneous leishmaniasis (ACL) is a protozoan parasitic disease caused by different Leishmania spp. from L. (Leishmania) and L. (Viannia) subgenera. In Brazil, seven Leishmania spp. act as ACL agents. Infection with L. (L.) amazonensis presents a wide clinical-immunopathological spectrum, ranging from localized cutaneous leishmaniasis (LCL), which usually responds well to antimony therapy, to borderline disseminated cutaneous leishmaniasis (BDCL), which may require twice as much LCL-antimony therapy to cure, and, finally, to anergic diffuse cutaneous leishmaniasis (ADCL), which is highly resistant to any chemotherapy. This clinical variability is driven by different degrees of T-cell immunosuppression, which negatively impact delayed-type hypersensitivity (DTH), as assessed by the Montenegro skin test (MST).
Methods:
Given MST's role as a T-cell-mediated resistance marker, we used it for diagnosing and monitoring patients with LCL (n = 8) and BDCL (n = 3) due to L. (L.) amazonensis to assess T-cell immunosuppression in these patients. MST was assessed at diagnosis and after treatment, although one patient with LCL refused treatment. The study took place at the Evandro Chagas Institute (Pará, Brazil), with diagnosis confirmed through parasitological assays, MST using L. (V.) braziliensis antigen, indirect fluorescent antibody test (IFAT)-immunoglobulin (Ig)G serology, histopathology, and PCR. Phenotypic and genotypic analyses were used to identify the primary agent.
Results:
MST was negative in all patients, both before and after successful treatment. Notably, one patient with LCL who declined treatment also showed no MST reactivity both before and after spontaneous healing. The absence of MST reactivity persisted for up to 1 year postcure in LCL and up to 2 years in BDCL, indicating a sustained lack of MST reactivity regardless of treatment outcome or spontaneous healing.
Conclusions:
The lack of MST reactivity pre- and post-treatment in LCL and BDCL challenges the role of DTH as a marker for T-cell-mediated resistance to L. (L.) amazonensis infection. Moreover, the first case of spontaneous LCL cure by L. (L.) amazonensis showed no MST reactivity pre- or post-resolution, raising doubts about the role of DTH in this process.
