CV Lattes
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Universidade de São Paulo (USP). Faculdade de Medicina (FM) (Institutional affiliation from the last research proposal) Birthplace: Brazil
She holds a degree in Biological Sciences - Medical Modality from the University of Santo Amaro (1981), a master's degree in Experimental and Comparative Pathology from the University of São Paulo (1993), a doctorate in Experimental and Comparative Pathology from the University of São Paulo (1998), and a Habilitation (Livre Docência) from the Department of Pathology of the Faculty of Veterinary Medicine and Animal Science of USP (2010). She is currently an Associate Professor in the Department of Pathology at the Faculty of Medicine of the University of São Paulo. She has experience in the field of Medicine and Veterinary Medicine, with an emphasis on Anatomical Pathology and Clinical Pathology, mainly working on the following topics: human, canine, and experimental visceral and cutaneous leishmaniasis, addressing the immunopathology of the infection, diagnosis, treatment, and immunization. Head of the Infectious Diseases Pathology Laboratory of the Department of Pathology at FMUSP (LIM-50), Coordinator of the Postgraduate Program in Experimental Physiopathology at FMUSP, Member of the Postgraduate Committee at FMUSP, Member of the Department of Pathology Council at FMUSP, Member of the Research Committee of the Department of Pathology at FMUSP, Member of the Research Committee at FMUSP, and Member of the Board of Directors of the Institute of Tropical Medicine at FMUSP. (Source: Lattes Curriculum)
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The dermotropic species of Leishmania cause a wide spectrum of clinical manifestations ranging from benign cutaneous lesions (ulcerated or not) to desfiguring and severe manifesations such as muco-cutaneous and disseminated. Brazil, especially in the Amazon, is considered the area with the highest biodiversity of Leishmania species. Some of them are rare and not well studied. In this proj…
In both Hansen's disease and American Tegumentary Leishmaniasis (ATL) there is two distinct (extreme) clinical status characterized by an intense chronic inflammatory cellular exudate with low parasite tissue load, as follow: Tuberculoid Hansen's disease (HT) and mucocutaneous leishmaniasis (CML). In general, even considering the particularities of each disease, it can be said that both s…
(Only some records are available in English at this moment)
The infection by Leishmania infantum causes visceral leishmaniasis in the New and Old World, which is fatal if not treated. Bisedes that, in some countries of Central America, L. infantum is able to cause an atypical clinical manifestation called non-ulcerated cutaneous leishmaniasis, different from that cause by the same specie of parasite in South America and Europe that is characterize…
Exploration of the genetic basis of Visceral Leishmaniasis (VL) has identified substantial amounts of biomarkers and thus has contributed to improve understanding of the pathogenesis of the VL. However, such findings have not been converted into disease control strategies. The identification of immunotherapeutic targets depends on the identification of metabolic pathways of the host, cons…
In the Americas, particularly in South America, infection by Leishmania (Leishmania) infantum chagasi cause subclinical manifestations and Visceral Leishmaniasis (VL), which if untreated is potentially fatal. In Honduras, infection by Leishmania (L.) infantum chagasi causes Visceral Leishmaniasis (VL), but has also been reported Non-Ulcerated or Atypical Cutaneous Leishmaniasis (NUCL) cau…
In the Americas, especially in South America, infection with Leishmania (Leishmania) infantum chagasi causes subclinical manifestations and visceral leishmaniasis (LV), which when untreated is potentially fatal. In Honduras, infection by Leishmania (L.) infantum chagasi causes Visceral Leishmaniasis (VL), but non-ulcerated or atypical cutaneous leishmaniasis (LCNU) caused by this parasite…
(Only some records are available in English at this moment)
Genetic diversity of the host-parasite interplay may be associated with differences in disease outcome, resistance to treatment and eco-epidemiological traits. Deletion of a >12kb loci on chromosome 31 of L. infantum has been associated with resistance to treatment in visceral leishmaniasis (VL). Named Mitelfosine Sensitive Loci (MSL), this chromosomal segment includes genes related to vi…