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Imaging the development of chronic Chagas disease after oral transmission

Chagas disease is a zoonosis caused by the protozoan parasite Trypanosoma cruzi. Transmission cycles are maintained by haematophagous triatomine bug vectors that carry infective T. cruzi in their faeces. Most human infections are acquired by contamination of mucosal membranes with triatomine faeces...

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Autores principales: Lewis, Michael D., Francisco, Amanda F., Jayawardhana, Shiromani, Langston, Harry, Taylor, Martin C., Kelly, John M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062536/
https://www.ncbi.nlm.nih.gov/pubmed/30050153
http://dx.doi.org/10.1038/s41598-018-29564-7
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author Lewis, Michael D.
Francisco, Amanda F.
Jayawardhana, Shiromani
Langston, Harry
Taylor, Martin C.
Kelly, John M.
author_facet Lewis, Michael D.
Francisco, Amanda F.
Jayawardhana, Shiromani
Langston, Harry
Taylor, Martin C.
Kelly, John M.
author_sort Lewis, Michael D.
collection PubMed
description Chagas disease is a zoonosis caused by the protozoan parasite Trypanosoma cruzi. Transmission cycles are maintained by haematophagous triatomine bug vectors that carry infective T. cruzi in their faeces. Most human infections are acquired by contamination of mucosal membranes with triatomine faeces after being bitten, however, T. cruzi can be transmitted by several other routes. Oral transmission is an increasingly important aspect of Chagas disease epidemiology, typically involving food or drink products contaminated with triatomines. This has recently caused numerous outbreaks and been linked to unusually severe acute infections. The long-term impact of oral transmission on infection dynamics and disease pathogenesis is unclear. We used highly sensitive bioluminescence imaging and quantitative histopathology to study orally transmitted T. cruzi infections in mice. Both metacyclic and bloodform trypomastigotes were infectious via the oral cavity, but only metacyclics led to established infections by intra-gastric gavage. Mice displayed only mild acute symptoms but later developed significantly increased myocardial collagen content (p = 0.017), indicative of fibrosis. Gastrointestinal tissues and skin were the principal chronic infection reservoirs. Chronic phase parasite load profiles, tissue distribution and myocardial fibrosis severity were comparable to needle-injected controls. Thus, the oral route neither exacerbates nor ameliorates experimental Chagas disease.
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spelling pubmed-60625362018-07-31 Imaging the development of chronic Chagas disease after oral transmission Lewis, Michael D. Francisco, Amanda F. Jayawardhana, Shiromani Langston, Harry Taylor, Martin C. Kelly, John M. Sci Rep Article Chagas disease is a zoonosis caused by the protozoan parasite Trypanosoma cruzi. Transmission cycles are maintained by haematophagous triatomine bug vectors that carry infective T. cruzi in their faeces. Most human infections are acquired by contamination of mucosal membranes with triatomine faeces after being bitten, however, T. cruzi can be transmitted by several other routes. Oral transmission is an increasingly important aspect of Chagas disease epidemiology, typically involving food or drink products contaminated with triatomines. This has recently caused numerous outbreaks and been linked to unusually severe acute infections. The long-term impact of oral transmission on infection dynamics and disease pathogenesis is unclear. We used highly sensitive bioluminescence imaging and quantitative histopathology to study orally transmitted T. cruzi infections in mice. Both metacyclic and bloodform trypomastigotes were infectious via the oral cavity, but only metacyclics led to established infections by intra-gastric gavage. Mice displayed only mild acute symptoms but later developed significantly increased myocardial collagen content (p = 0.017), indicative of fibrosis. Gastrointestinal tissues and skin were the principal chronic infection reservoirs. Chronic phase parasite load profiles, tissue distribution and myocardial fibrosis severity were comparable to needle-injected controls. Thus, the oral route neither exacerbates nor ameliorates experimental Chagas disease. Nature Publishing Group UK 2018-07-26 /pmc/articles/PMC6062536/ /pubmed/30050153 http://dx.doi.org/10.1038/s41598-018-29564-7 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Lewis, Michael D.
Francisco, Amanda F.
Jayawardhana, Shiromani
Langston, Harry
Taylor, Martin C.
Kelly, John M.
Imaging the development of chronic Chagas disease after oral transmission
title Imaging the development of chronic Chagas disease after oral transmission
title_full Imaging the development of chronic Chagas disease after oral transmission
title_fullStr Imaging the development of chronic Chagas disease after oral transmission
title_full_unstemmed Imaging the development of chronic Chagas disease after oral transmission
title_short Imaging the development of chronic Chagas disease after oral transmission
title_sort imaging the development of chronic chagas disease after oral transmission
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062536/
https://www.ncbi.nlm.nih.gov/pubmed/30050153
http://dx.doi.org/10.1038/s41598-018-29564-7
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