Epidemiological Aspects of Chagas Disease - a Review

Abstract

Chagas disease (ChD), also known as American trypanosomiasis, is caused by the trypanosomatid protozoan Trypanosoma cruzi (T. cruzi) that in its natural life-cycle is transmitted through triatomine vectors. Parasitological studies are useful to confirm acute cases, while the diagnosis of chronic T. cruzi infection relies on serological methods. There is no vaccine to prevent the infection, and the treatment is restricted to nifurtimox and benznidazole; and hence, new effective drugs with lower side-effects are urgently needed. The current review updates the facts and phenomena related to ChD, which is becoming an emerging health problem in non-endemic areas too, making the disease a grave global concern.

Conservation and divergence within the clathrin interactome of Trypanosoma cruzi

“…In trypanosomatids, a group of pathogenic protozoa afflicting much of the world’s population, clathrin-based trafficking represents an important interface with the host and plays multiple roles in immune evasion and host cell invasion vital for effective infection and persistence 11 . The American trypanosome, Trypanosoma cruzi, is both a hemoflagellate and intracellular pathogen and causes Chagas disease in South and Central America 12 . All evidence is consistent with clathrin-mediated endocytosis (CME) being restricted to the flagellar pocket, a common feature of trypanosomatids 13 .…”

Desarrollo preclínico de vacunas profilácticas contra la Enfermedad de Chagas basadas en Transialidasa.

“…El parásito a lo largo de su ciclo de vida alterna entre el insecto vector y huéspedes mamíferos. Según el hospedero en el que se encuentre, T. cruzi adopta diferentes formas biológicas, las cuales se caracterizan por las posiciones relativas del flagelo, el cinetoplasto y el núcleo; y son funcionalmente distintas (6,7). La forma epimastigote se localiza en el tracto digestivo del vector, se identifica por presentar un cinetoplasto alargado y es una forma replicativa (7,8).…”

“…Según el hospedero en el que se encuentre, T. cruzi adopta diferentes formas biológicas, las cuales se caracterizan por las posiciones relativas del flagelo, el cinetoplasto y el núcleo; y son funcionalmente distintas (6,7). La forma epimastigote se localiza en el tracto digestivo del vector, se identifica por presentar un cinetoplasto alargado y es una forma replicativa (7,8). La forma tripomastigote se caracteriza por presentar un cinetoplasto localizado por detrás del núcleo, el flagelo nace en su proximidad y emerge por un costado del cuerpo del parásito.…”

Quantitative Structure–Activity Relationships for Structurally Diverse Chemotypes Having Anti-Trypanosoma cruzi Activity

“…Replicative epimastigotes and infective metacyclic trypomastigotes develop in Triatomine bugs, whereas replicative intracellular amastigotes and non-replicative bloodstream trypomastigotes develop in humans [6]. Intracellular amastigotes, which are found in tissues such as cardiac muscles and the digestive system, are the clinically relevant form of the parasite, and thus are the targets of antichagasic agents [6,7]. Occasionally, compounds that are active against isolated macromolecular targets lose their activity when tested in whole-cell phenotypic assays [8,9,10,11].…”