Observations on the development of Trypanosoma rangeli in the hemocoel of Rhodnius prolixus |
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| Authors: | E J Tobie |
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| Affiliation: | 1. Center for Clinical Epidemiology and Biostatistics, Department of Biostatistics and Epidemiology, Perelman School of Medicine, University of Pennsylvania, PA, USA;2. Facultad de Ciencias y Filosofía, Universidad Peruana Cayetano Heredia, Lima, Peru;1. Grupo de Ciencias Básicas, Facultad de Medicina, Universidad de Los Andes, Bogotá, DC, Colombia;2. Grupo de Biofísica, Departamento de Física, Universidad de los Andes, Bogotá, DC, Colombia;3. Núcleo de Biotecnología Curauma, Pontificia Universidad Católica Valparaíso, Valparaíso, Chile;4. Instituto de Parasitología y Biomedicina López Neyra, Consejo Superior de Investigaciones Científicas (IPBLN-CSIC) P.T. de Ciencias de la Salud, Granada, Spain;5. Grupo de Inmunobiología y Biología Celular, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, DC, Colombia;6. Laboratorio de Parasitología Molecular, Departamento de microbiología, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, DC, Colombia |
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| Abstract: | The development of Trypanosoma rangeli in the hemocoel of Rhodnius prolixus was studied with the idea of elucidating the function of the forms found there. When flagellates from cultures of T. rangeli that have decreased in virulence are introduced into the hemocoel of R. prolixus the salivary glands are not invaded regularly or, if invaded, the infection does not persist. However, the parasite lives and multiplies in the hemocoel. Crithidial forms enter the plasmotocytes where they roll up and divide. This hemocyte becomes greatly enlarged due to the dividing leishmania forms within its cytoplasm. Eventually the cell ruptures releasing numerous crithidias, some of which transform into trypanosomes as evidenced by the presence of metacyclic as well as long forms. These observations also help explain the pathogenic action of T. rangeli to its invertebrate host. |
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