141 research outputs found
Casos autóctones da Doença de Chagas em Santa Catarina: diagnosticados em Floriaópolis no período de janeiro de 1970 a abril de 1987.
No full textTrabalho de Conclusão de Curso - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Departamento de Clínica Médica, Curso de Medicina, Florianópolis, 198
North American import? Charting the origins of an enigmatic Trypanosoma cruzi domestic genotype.
No full textBACKGROUND: Trypanosoma cruzi, the agent of Chagas disease, is currently recognized as a complex of six lineages or Discrete Typing Units (DTU): TcI-TcVI. Recent studies have identified a divergent group within TcI - TcI(DOM). TcI(DOM). is associated with a significant proportion of human TcI infections in South America, largely absent from local wild mammals and vectors, yet closely related to sylvatic strains in North/Central America. Our aim was to examine hypotheses describing the origin of the TcI(DOM) genotype. We propose two possible scenarios: an emergence of TcI(DOM) in northern South America as a sister group of North American strain progenitors and dispersal among domestic transmission cycles, or an origin in North America, prior to dispersal back into South American domestic cycles. To provide further insight we undertook high resolution nuclear and mitochondrial genotyping of multiple Central American strains (from areas of México and Guatemala) and included them in an analysis with other published data. FINDINGS: Mitochondrial sequence and nuclear microsatellite data revealed a cline in genetic diversity across isolates grouped into three populations: South America, North/Central America and TcI(DOM). As such, greatest diversity was observed in South America (A(r) = 4.851, π = 0.00712) and lowest in TcI(DOM) (Ar = 1.813, π = 0.00071). Nuclear genetic clustering (genetic distance based) analyses suggest that TcI(DOM) is nested within the North/Central American clade. CONCLUSIONS: Declining genetic diversity across the populations, and corresponding hierarchical clustering suggest that emergence of this important human genotype most likely occurred in North/Central America before moving southwards. These data are consistent with early patterns of human dispersal into South America
DIRETRIZ DA SOCIEDADE BRASILEIRA DE CARDIOLOGIA E DA SOCIEDADE BRASILEIRA DE HEMODINÂMICA E CARDIOLOGIA INTERVENCIONISTA SOBRE INTERVENÇÃO CORONÁRIA PERCUTÂNEA
No full textInst Dante Pazzanese Cardiol, Sao Paulo, SP, BrazilUniv Sao Paulo, Fac Med, Hosp Clin, Ribeirao Preto, SP, BrazilHosp Coracao Anis Rassi, Goiania, Go, BrazilInst Coracao Triangulo, Uberlandia, MG, BrazilEscola Paulista Med, Sao Paulo, SP, BrazilHosp Felicio Rocho, Belo Horizonte, MG, BrazilReal & Benemerita Soc Portuguesa Beneficencia, Sao Paulo, SP, BrazilUniv Sao Paulo, Fac Med, Inst Coracao, Hosp Clin, Sao Paulo, SP, BrazilFundacao Univ Cardiol, Inst Cardiol Rio Grande do Sul, Porto Alegre, RS, BrazilHosp Santa Paula, Cardioctr, Joao Pessoa, Paraiba, BrazilHosp Bandeirantes, Sao Paulo, SP, BrazilClin Sao Vicente, Rio De Janeiro, RJ, BrazilUniv Fed Sao Paulo, Escola Paulista Med, Sao Paulo, SP, BrazilWeb of Scienc
Análise econômica dos Stents coronarianos farmacológicos no Brasil: para todos ou para poucos pacientes? Economic analysis of drug-eluting coronary stents in Brazil: a choice for all or just for a few patients?
No full textSystematic review of in vitro and in vivo infections by Trypanosoma cruzi: the role of reactive oxygen species in amastigote intracellular multiplication
No full textTrypanosoma cruzi is the causative agent of Chagas disease (American trypanosomiasis), a neglected and multifactorial condition, which affects about seven million people around the world (WHO, 2021). Chagas disease is characterized by two phases: acute and chronic. The first lasts from two to four months, a period in which the parasitemia is detectable and its symptoms are generally mild (Chagas, 1916; Dutra et al., 2009). Acute symptomatic cases are rare, less than 5-10% of the affected evolve to death, the latter are usually related to myocarditis, meningoencephalitis or both (Rassi Jr. A.; Rassi, A.; Marin-Neto, 2010). Although the majority of chronic infected individuals are asymptomatic, about 40% of them progress to severe cardiac, digestive or mixed manifestations (WHO, 2021; Rassi Jr. A.; Rassi, A.; Marin-Neto, 2010).
T. cruzi is a tripanosomatid protozoan parasite capable of infecting a plethora of nucleated cells. The lifecycle of this organism is complex and consists of various stages and intermediate forms (Chagas, 1909; Brener, 1965, 1969; Souza & Barrias, 2020). The classical ones are the epimastigote (insect infective and proliferative), trypomastigote (mammalian infective) and amastigote (intracellular proliferative) stages (Chagas, 1909). T. cruzi is genetically divided into discrete typing units (DTUs) that encompass several strains (Zingales, 2009), with different behavior in their infected host cells.
T. cruzi relation with its intracellular micro-ambient is fundamental for Chagas disease development. The effect of reactive oxygen species (ROS) on that protozoan is controversial. Oxidative stress may be toxic, causing parasite death and/or inhibition of proliferation (Romaña & Meyer, 1942; Tanaka; Tanowitz; Bloom, 1983; Piacenza, et al. 2007), but there are also evidences showing that those molecules may favor trypomastigote differentiation and amastigote multiplication, contributing to T. cruzi lifecycle maintenance (Paiva et al. 2012; Dias et al. 2017; Paula et al. 2020). Since this controversy remains, the current study aims to clarify the role of ROS in the amastigote stage of this protozoan parasite.
We plan to identify how intracellular environment (pro-oxidant/antioxidant) affects parasite multiplication and the level of oxidative stress necessary to provide that effect, reviewing all available literature of preclinical research (in vitro and in vivo) in form of a Systematic Review. This approach was chosen taking into consideration the character of neglected disease which American trypanosomiasis presents and the urge to improve bench-bedside translation for the population affected by this disease. In vitro/in vivo systematic reviews are relatively new and have potential to identify methodological quality, gaps of knowledge and potential biases, justifying its use (Sena et al. 2014)
El misterio de la enfermedad de Chagas
No full textAlguna vez hemos escuchado el término “enfermedad de Chagas (EC)”, sin embargo, la mayoría de nosotros no hacemos caso sobre el asunto. Excepto por algunas frases que se han convertido en la ventana de entrada de información para ésta: “qué curioso animal, le llaman chinche besucona”, “¿un parásito es algo que se alimenta de mí?”, “no puede ser tan grave que me pique un animal así (haciendo referencia al vector que la causa)”, entre otras. Por cierto, es importante recordar que el término “vector” hace referencia a cualquier agente que transporta y transmite, en este caso, el parásito que la ocasiona (Rassi Jr. et al., 2010)
Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial
No full textChagas cardiomyopathy is the most frequent and most severe manifestation of chronic Chagas disease, and is one of the leading causes of morbidity and death in Latin America. Although the pathogenesis of Chagas cardiomyopathy is incompletely understood, it may involve several mechanisms, including parasite-dependent myocardial damage, immune-mediated myocardial injury (induced by the parasite itself and by self-antigens), and microvascular and neurogenic disturbances. In the past three decades, a consensus has emerged that parasite persistence is crucial to the development and progression of Chagas cardiomyopathy. In this context, antiparasitic treatment in the chronic phase of Chagas disease could prevent complications related to the disease. However, according to the results of the BENEFIT trial, benznidazole seems to have no benefit for arresting disease progression in patients with chronic Chagas cardiomyopathy. In this review, we give an update on the main pathogenic mechanisms of Chagas disease, and re-examine and discuss the results of the BENEFIT trial, together with its limitations and implications
Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification
No full textChagas heart disease (CHD) results from infection with the protozoan parasite Trypanosoma cruzi and is the leading cause of infectious myocarditis worldwide. It poses a substantial public health burden due to high morbidity and mortality. CHD is also the most serious and frequent manifestation of chronic Chagas disease and appears in 20-40% of infected individuals between 10-30 years after the original acute infection. In recent decades, numerous clinical and experimental investigations have shown that a low-grade but incessant parasitism, along with an accompanying immunological response [either parasite-driven (most likely) or autoimmune-mediated], plays an important role in producing myocardial damage in CHD. At the same time, primary neuronal damage and microvascular dysfunction have been described as ancillary pathogenic mechanisms. Conduction system disturbances, atrial and ventricular arrhythmias, congestive heart failure, systemic and pulmonary thromboembolism and sudden cardiac death are the most common clinical manifestations of chronic Chagas cardiomyopathy. Management of CHD aims to relieve symptoms, identify markers of unfavourable prognosis and treat those individuals at increased risk of disease progression or death. This article reviews the pathophysiology of myocardial damage, discusses the value of current risk stratification models and proposes an algorithm to guide mortality risk assessment and therapeutic decision-making in patients with CHD
Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial
No full textChallenges and opportunities for primary, secondary, and tertiary prevention of Chagas' disease
No full textA century after its discovery, Chagas' disease still represents a major public health challenge in Latin America. Moreover, because of growing population movements, an increasing number of cases of imported Chagas' disease have now been detected in non-endemic areas, such as North America and some European countries. This parasitic zoonosis, caused by Trypanosoma cruzi, is transmitted to humans by infected Triatominae insects, or occasionally by non-vectorial mechanisms, such as blood transfusion, mother to fetus, or oral ingestion of materials contaminated with parasites. Following the acute phase of the infection, untreated individuals enter a chronic phase that is initially asymptomatic or clinically unapparent. Usually, a few decades later, 40-50% of patients develop progressive cardiomyopathy and/or motility disturbances of the oesophagus and colon. In the last decades several interventions targeting primary, secondary and tertiary prevention of Chagas' disease have been attempted. While control of both vectorial and blood transfusion transmission of T cruzi (primary prevention) has been successful in many regions of Latin America, early detection and aetiological treatment of asymptomatic subjects with Chagas' disease (secondary prevention) have been largely underutilised. At the same time, in patients with established chronic disease, several pharmacological and non-pharmacological interventions are currently available and have been increasingly used with the intention of preventing or delaying complications of the disease (tertiary prevention). In this review we discuss in detail each of these issues
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