VERA LUCIA TEIXEIRA DE FREITAS
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Moléstias Infecciosas e Parasitárias, Faculdade de Medicina
LIM/48 - Laboratório de Imunologia, Hospital das Clínicas, Faculdade de Medicina
LIM/48 - Laboratório de Imunologia, Hospital das Clínicas, Faculdade de Medicina
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
- Suspected vertical transmission of Chagas disease caused by DTU TcIV in an infection probably transmitted orally, during anoutbreak in the Brazilian Amazon(2021) FREITAS, Vera Lucia Teixeira de; ESPER, Helena Rangel; NAKANISHI, Erika Shimoda; PIOTTO, Mariana Ramos; ASSY, Joao Guilherme Pontes Lima; BERRETA, Olivia Campos Pinheiro; SAID, Renato do Carmo; SEGURADO, Aluisio Augusto Cotrim; CARVALHO, Noemia Barbosa; FRANCA, Francisco Oscar de Siqueira; LOPES, Marta HeloisaThis study describes difficulties in the monitoring of a child born during an oral outbreak of Chagas disease, in which there are several indications that the transmission occurred through the congenital route: 1. the mother was in the third trimester of pregnancy when she was infected; 2. She presented high parasitemia at the time of delivery; 3. In both, the mother and her daughter, T cruzi was classified as DTU TcIV. The parasites were not found in the blood at birth and the infection was detected only three months later in an asymptomatic infant. As the mother and her child live in a highly endemic area, vector transmission could not be excluded during this period.
- Fatal evolution of acute Chagas disease in a child from Northern Brazil: factors that determine poor prognosis(2019) ESPER, Helena Rangel; FREITAS, Vera Lucia Teixeira de; ASSY, Joao Guilherme Pontes Lima; SHIMODA, Erika Yoshie; BERRETA, Olivia Campos Pinheiro; LOPES, Marta Heloisa; FRANCA, Francisco Oscar SiqueiraTrypanosoma cruzi is the causative agent of Chagas disease. Nowadays, the transmission in Brazil occurs mainly by oral ingestion of contaminated food that has been associated with more severe clinical manifestations. We report a case of Acute Chagas disease caused by oral transmission in a child from Northern Brazil. In the hospital admission, physical examination showed tachycardia, hepatomegaly. bipalpebral edema and anasarca. Trypanosoma cruzi trypomastigotes were found in microscopy during blood cell count. Twenty-three days before hospitalization, the child had ingested the ""bacaba palm fruit's wine"". Even with the appropriate diagnosis and starting of treatment, she did not survive. Quantitative analysis of Trypanosoma cruzi DNA in a blood sample resulted in 54,053.42 parasite equivalents/mL and the DTU TcIV was identified. The outcome may have been determined by several factors, including the delay to seek a medical service beyond the high parasitemia, detected by qPCR. DTU TcIV could also have influenced the natural history of the disease.
- Role of T. cruzi exposure in the pattern of T cell cytokines among chronically infected HIV and Chagas disease patients(2017) TOZETTO-MENDOZA, Tania Regina; VASCONCELOS, Dewton de Moraes; IBRAHIM, Karim Yaqub; SARTORI, Ana Marli Christovam; BEZERRA, Rita C.; FREITAS, Vera Lucia Teixeira de; SHIKANAI-YASUDA, Maria AparecidaOBJECTIVES: The impact of Chagas disease (CD) in HIV-infected patients is relevant throughout the world. In fact, the characterization of the adaptive immune response in the context of co-infection is important for predicting the need for interventions in areas in which HIV and Chagas disease co-exist. METHODS: We described and compared the frequency of cytokine-producing T cells stimulated with soluble antigen of Trypanosoma cruzi (T. cruzi) using a cytometric assay for the following groups: individuals with chronic Chagas disease (CHR, n=10), those with Chagas disease and HIV infection (CO, n=11), those with only HIV (HIV, n=14) and healthy individuals (C, n=15). RESULTS: We found 1) a constitutively lower frequency of IL-2+ and IFN-gamma+T cells in the CHR group compared with the HIV, CO and healthy groups; 2) a suppressive activity of soluble T. cruzi antigen, which down-regulated IL-2+CD4+ and IFN-gamma+ CD4+ phenotypes, notably in the healthy group; 3) a down-regulation of inflammatory cytokines on CD8+ T cells in the indeterminate form of Chagas disease; and 4) a significant increase in IL-10 + CD8+ cells distinguishing the indeterminate form from the cardiac/digestive form of Chagas disease, even in the presence of HIV infection. CONCLUSIONS: Taken together, our data suggest the presence of an immunoregulatory response in chronic Chagas disease, which seems to be driven by T. cruzi antigens. Our findings provide new insights into immunotherapeutic strategies for people living with HIV/AIDS and Chagas disease.
- Aplastic Anemia and Chagas Disease: T. cruzi Parasitemia Monitoring by Quantitative PCR and Preemptive Antiparasitic Therapy(2022) CARVALHO, Noemia Barbosa; FREITAS, Vera Teixeira de; BEZERRA, Rita Cristina; NAKANISHI, Erika Shimoda; VELLOSO, Elvira Pereira; HIGASHINO, Hermes Ryoiti; BATISTA, Marjorie Vieira; FONSECA, Guilherme Henrique; ROCHA, Vanderson; COSTA, Silvia Figueiredo; SHIKANAI-YASUDA, Maria AparecidaBackground: Aplastic anemia is a rare and life-threatening condition, seldomly witnessed concomitantly with Chagas disease. We aim to discuss the management of these patients under risk of chronic Chagas disease reactivation (CDR), a severe condition with a high morbimortality that occurs in chronic Chagas disease patients under immunosuppression. Case reports: Trypanosoma cruzi (T. cruzi) parasitemia was monitored in three patients for 4-58 months by conventional PCR (cPCR), quantitative PCR (qPCR), microhematocrit/buffy coat, blood culture, and/or xenodiagnosis. One patient received antiparasitic treatment (benznidazole) and the other received allopurinol. Although parasitemia was controlled during and after benznidazole treatment at 300 mg/d for 51 days, in one patient, hematologic parameters worsened continuously before, during, and after treatment. Allopurinol led only to the temporary suppression of T. cruzi parasitemia in the second patient, but after danazol and hematological improvement, parasitemia became undetectable until the end of monitoring. Discussion and Conclusion: Unexpected undetectable or low parasitemia by cPCR/qPCR was reported. We show that the monitoring of parasitemia by qPCR and the use of preemptive therapy when the parasitemia was positive proved to be beneficial to our patients. As a result of the toxicity of more effective antiparasitics, shorter regimens of benznidazole or less toxic drugs in preemptive therapy are options that deserve future studies.
- Real-Time PCR in HIV/Trypanosoma cruzi Coinfection with and without Chagas Disease Reactivation: Association with HIV Viral Load and CD4(+) Level(2011) FREITAS, Vera Lucia Teixeira de; SILVA, Sheila Cristina Vicente da; SARTORI, Ana Marli; BEZERRA, Rita Cristina; WESTPHALEN, Elizabeth Visone Nunes; MOLINA, Tatiane Decaris; TEIXEIRA, Antonio R. L.; IBRAHIM, Karim Yaqub; SHIKANAI-YASUDA, Maria AparecidaBackground: Reactivation of chronic Chagas disease, which occurs in approximately 20% of patients coinfected with HIV/Trypanosoma cruzi (T. cruzi), is commonly characterized by severe meningoencephalitis and myocarditis. The use of quantitative molecular tests to monitor Chagas disease reactivation was analyzed. Methodology: Polymerase chain reaction (PCR) of kDNA sequences, competitive (C-) PCR and real-time quantitative (q) PCR were compared with blood cultures and xenodiagnosis in samples from 91 patients (57 patients with chronic Chagas disease and 34 with HIV/T. cruzi coinfection), of whom 5 had reactivation of Chagas disease and 29 did not. Principal Findings: qRT-PCR showed significant differences between groups; the highest parasitemia was observed in patients infected with HIV/T. cruzi with Chagas disease reactivation (median 1428.90 T. cruzi/mL), followed by patients with HIV/T. cruzi infection without reactivation (median 1.57 T. cruzi/mL) and patients with Chagas disease without HIV (median 0.00 T. cruzi/mL). Spearman's correlation coefficient showed that xenodiagnosis was correlated with blood culture, C-PCR and qRT-PCR. A stronger Spearman correlation index was found between C-PCR and qRT-PCR, the number of parasites and the HIV viral load, expressed as the number of CD4(+) cells or the CD4(+)/CD8(+) ratio. Conclusions: qRT-PCR distinguished the groups of HIV/T. cruzi coinfected patients with and without reactivation. Therefore, this new method of qRT-PCR is proposed as a tool for prospective studies to analyze the importance of parasitemia (persistent and/or increased) as a criterion for recommending pre-emptive therapy in patients with chronic Chagas disease with HIV infection or immunosuppression. As seen in this study, an increase in HIV viral load and decreases in the number of CD4(+) cells/mm(3) and the CD4(+)/CD8(+) ratio were identified as cofactors for increased parasitemia that can be used to target the introduction of early, pre-emptive therapy.