Kinetoplastid Biology and Disease最新文献

At times of crisis when epidemics rage and begin to take their toll on affected populations, as we have been witnessing with African trypanosomiasis in subSahara, the dichotomy of basic versus applied research deepens. While undoubtedly the treatment of thousands of infected people is the top priority, without continued research and development on the biology of disease agents and on ecological and evolutionary forces impacting these epidemics, little progress can be gained in the long run for the eventual control of these diseases. Here, we argue the need for additional research in one under-investigated area, that is the biology of the tsetse vector. Lacking are studies aimed to understand the genetic and cellular basis of tsetse interactions with trypanosomes as well as the genetic and biochemical basis of its ability to transmit these parasites. We discuss how this knowledge has the potential to contribute to the development of new vector control strategies as well as to improve the efficacy and affordability of the existing control approaches.

Members of the Trypanosomatidae family comprise a large number of species that are causative agents of important diseases such as sleeping sickness, Chagas' disease and Leishmaniasis. These organisms are also of biological interest since they are able to change the morphology according to the environment where they live, through a process of reversible cell transformation, and possess structures and organelles that are not found in mammalian cells. This review analyses the process of transformation, which takes place during the life cycle of Trypanosoma cruzi in the vertebrate and invertebrate hosts. Special attention is given to the interaction of the parasite with vertebrate cells. In addition, the present knowledge of structures and organelles such as the nucleus, the plasma membrane, the sub-pellicular microtubules, the flagellum, the kinetoplast-mitochondrion complex, the peroxisome (glycosome), the acidocalcisome and the structures and organelles involved in the endocytic pathway, is reviewed from a cell biology perspective. The possible use of available data for the development of new anti parasite drugs is also discussed.

Trypanosoma (Herpetosoma) lewisi is a trypanosome of the sub-genus Herpetosoma (Stercoraria section), parasite of rats (Rattus rattus and Rattus norvegicus) transmitted by fleas. T. lewisi has a stringent species specificity and cannot grow in other rodents such as mice. Rats are infected principally by oral route, through contamination by flea faeces or ingestion of fleas. Trypanosoma lewisi infections in rat colonies can interfere with research protocols and fleas of wild rats are often the source of such infections. Currently, diagnosis of T. lewisi in rats is performed by microscopic observation of stained blood smears. In the course of a research project at CIRDES, a T. lewisi infection was detected in the rat colony. In this study we evaluated PCR primer sets for their ability to diagnose multiple species of trypanosomes with a single amplification. We show that the use of ITS1 sequence of ribosomal DNA provides an efficient and sensitive assay for detection and identification of T. lewisi infection in rats and recommend the use of this assay for monitoring of T. lewisi infections in rat colonies.

A Leishmania model to explain microbial virulence in chronic infectious diseases is proposed. All these diseases progress from infection to symptomatic phase to host death or recovery. The outcome of each phase is depicted to result from the interactions of a distinct group of parasite molecules with a specific host immune compartment. The first group consists of invasive/evasive determinants, which are largely parasite cell surface and secreted molecules. Their activities help parasites establish infection by overcoming host immunologic and non-immunologic barriers. These determinants do not cause disease per se, but are indispensable for infection necessary for the development of a disease-state. The second group of parasite molecules consists of "pathoantigenic" determinants - unique parasite epitopes present often within otherwise highly conserved cytoplasmic molecules. Immune response against these determinants is thought to result in immunopathology manifested as clinical signs or symptoms, namely the virulent phenotype. The third group of parasite molecules is hypothetically perceived as vaccine determinants. Their interactions with the host immune system lead to the elimination or reduction of parasites to effect a clinical cure. Differential expression of these determinants alone by parasites may alter their interactions with the hosts. Virulent phenotype is consequently presented as a spectrum of manifestations from asymptomatic infection to fatality. A secondary level of regulation lies in host genetic and environmental factors. The model suggests that different parasite determinants may be targeted by different strategies to achieve more effective control of leishmaniasis and other similar diseases.