New insights into Trypanosoma cruzi genetic diversity, and its influence on parasite biology and clinical outcomes.

Chagas disease, caused by Trypanosoma cruzi, remains a serious public health problem worldwide. The parasite was subdivided into six distinct genetic groups, called "discrete typing units" (DTUs), from TcI to TcVI. Several studies have indicated that the heterogeneity of T. cruzi species directly affects the diversity of clinical manifestations of Chagas disease, control, diagnosis performance, and susceptibility to treatment. Thus, this review aims to describe how T. cruzi genetic diversity influences the biology of the parasite and/or clinical parameters in humans. Regarding the geographic dispersion of T. cruzi, evident differences were observed in the distribution of DTUs in distinct areas. For example, TcII is the main DTU detected in Brazilian patients from the central and southeastern regions, where there are also registers of TcVI as a secondary T. cruzi DTU. An important aspect observed in previous studies is that the genetic variability of T. cruzi can impact parasite infectivity, reproduction, and differentiation in the vectors. It has been proposed that T. cruzi DTU influences the host immune response and affects disease progression. Genetic aspects of the parasite play an important role in determining which host tissues will be infected, thus heavily influencing Chagas disease's pathogenesis. Several teams have investigated the correlation between T. cruzi DTU and the reactivation of Chagas disease. In agreement with these data, it is reasonable to suppose that the immunological condition of the patient, whether or not associated with the reactivation of the T. cruzi infection and the parasite strain, may have an important role in the pathogenesis of Chagas disease. In this context, understanding the genetics of T. cruzi and its biological and clinical implications will provide new knowledge that may contribute to additional strategies in the diagnosis and clinical outcome follow-up of patients with Chagas disease, in addition to the reactivation of immunocompromised patients infected with T. cruzi.

Effect of the expression of CD62P and thrombin generation on patients using central venous catheters for hemodialysis.

The formation of thrombi in medical devices that come into contact with blood is a common cause of increased morbidity and mortality. Prolonged use of central venous catheters (CVCs) may cause high infection rates or compromise CVC patency due to thrombus development. In this study, we sought insights into possible changes in the hemostatic system during prolonged use of inserted CVCs for hemodialysis by assessing platelets by CD62P and CD41a expression and the potential for thrombin generation (TG). This study included patients with chronic renal failure who were undergoing hemodialysis three times a week using a CVC, and healthy subjects as controls. The participants were distributed into three groups: Group 1: clinically and laboratorially healthy individuals matched by sex and age to the patients (controls); Group II: patients who had completed 1 month of CVC insertion; and Group III: the same patients after they had completed 4 months of CVC insertion. Platelet activation analysis and TG evaluation were performed using blood samples obtained through two different accesses, that is, through a peripheral vein and directly from the CVC lumen. The data showed platelet activation and an increase in the generation of thrombin, particularly after 4 months of CVC use. The results also indicated that insertion of the catheter into the blood stream stimulated the intrinsic rather than the extrinsic pathway. Taken together, the data showed a direct relationship between the use of CVCs in hemodialysis patients and a state of hypercoagulability, most likely associated with endothelial damage and the contact of the medical device with blood components such as platelets and coagulation factors.