ABSTRACT
The traditional transmission pathways of Chagas' disease are vectorial, transfusional, transplacental and organ transplantation. However, oral transmission is gaining importance. The first evidence of oral transmission was reported in Brazil in 1965. Nowadays the oral route is the transmission mode in 50 percent of cases in the Amazon river zone. Oral infection is produced by the ingestion of infected triatomine bugs or their feces, undercooked meat from infested host animals and food contaminated with urine or anal secretion of infected marsupials. Therefore travelers to those zones should be advised about care to be taken with ingested food. In Chile, this new mode of transmission should be considered in public health policies.
Subject(s)
Animals , Humans , Chagas Disease/transmission , Food Contamination , Food Parasitology , Latin America , Trypanosoma cruzi/parasitologyABSTRACT
Chagas' disease is produced by the haemophlagelated protozoan Trypanosoma cruzi and transmitted by haematophages insects such as Triatoma infestans (vinchuca). Due to vector control, congenital transmission gains importance and is responsible for the presence and expansion of this disease in non-endemic areas. The mechanisms of congenital infection are uncertain. It has been suggested that the parasite reaches the fetus through the bloodstream by crossing the placental barrier, and that congenital Chagas' disease is the result of complex interactions between the immune response, placental factors, and the parasite's characteristics. We review the cellular and molecular mechanisms of infection and invasion of the parasite and how immune and placental factors may modulate this process. Finally, we propose a possible model for the vertical transmission of Chagas' disease.
Subject(s)
Animals , Female , Humans , Infant, Newborn , Pregnancy , Chagas Disease/congenital , Chagas Disease/transmission , Infectious Disease Transmission, Vertical , Pregnancy Complications, Parasitic/parasitology , Trypanosoma cruzi/physiology , Chagas Disease/parasitology , Host-Parasite Interactions , Placenta/parasitology , Trypanosoma cruzi/immunologyABSTRACT
Echinococcus granulosus is a parasitic platyhelminth that is responsible for cystic hydatid disease. From the inner, germinal layer of hydatid cysts protoscoleces are generated, which are are the infective forms to the dog. Systematic studies on the cell biology of E. granulosus protoscolex formation in natural infections are scarce and incomplete. In the present report we describe seven steps in the development of protoscoleces. Cellular buds formed by a clustering of cells emerge from the germinal layer of hydatid cysts. The buds elongate and the cells at their bases seem to diminish in number. Very early on a furrow appears in the elongated buds, delimiting anterior (scolex) and caudal (body) regions. Hooks are the first fully-differentiated structures formed at the apical region of the nascent scolex. In a more advanced stage, the scolex shows circular projections and depressions that develop into suckers. A cone can later be seen at the center of the hooks, the body is expanded and a structured neck is evident between the scolex and the body. During protoscolex development this parasitic form remains attached to the germinative layer through a stalk. When fully differentiated, the stalk is cut off and the infective protoscolex is now free in the hydatid fluid
Subject(s)
Animals , Echinococcosis , Echinococcus , Sheep Diseases , Echinococcosis , Echinococcus , Microscopy, Electron, Scanning , SheepABSTRACT
En este trabajo se describe la realización de un mapeo del genoma del parásito causal de la enfermedad de Chagas, el Trypanosoma cruzi, hibridando una genoteca construída en cósmidos y grillada en filtros de alta densidad, utilizando como sondas clones de AND copia provenientes de una genoteca de expresión en epimastigotes. Se muestra además la correlación de secuencias superpuestas de cósmidos (contigs) con bandas cromosomales del parásito. Utilizando estas mismas genotecas generadas por el Proyecto Genoma de T. cruzi, se caracterizó un nuevo miembro de la familia Tc 13 de la superfamilia de antígenos de superficie de tripomastigotes. A partir de un clon de la cepa Tulahuén stock. Tul2, con homología con estos antígenos, se secuenció y caracterizó el gen completo en la cepa de referencia CL clon CL Brener, encontrándose además homología con diferentes ESTs, lo cual posibilitaria conocer en su totalidad a esta familia de antígenos.
Subject(s)
Animals , Antigens, Protozoan/genetics , Antigens, Surface/genetics , Genome , Trypanosoma cruzi/genetics , Base Sequence , Chromosome Mapping , DNA Probes , KaryotypingABSTRACT
The organization of chromatin in protists presents some characteristic features. In Trypanosoma cruzi, no condensation of chromatin into chromosomes is observed during cell division. A systematic characterization of histones should provide information on this peculiar behaviour. Histone H2B from this parasite was characterized by selective dissociation from chromatin in 0.8 M NaCl, by its elution pattern in narrow-bore reversed phase high performance liquid chromatography, by polyacrylamide gel electrophoresis and by partial sequencing of its amino terminal domain. This chromosomal protein differs from histone H2B of other species. The first 12 amino acids are missing which explains its lower molecular weight when compared to human histone H2B. Correspondingly, the amino terminal domain of T. cruzi histone H2B is 25-30 percent shorter than other histones H2B. Moreover, three out of four acetylation sites present in human histone H2B are missing in T. cruzi histone H2B. The differences in size and in acceptor sites for acetylation of T. cruzi histone H2B when compared to human histone H2B may represent a functional feature to consider for the understanding of the chromatin cycle of condensation in this parasite