Imaging the development of chronic Chagas disease after oral transmission

Abstract 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 triatomin...

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Autores principales: Michael D. Lewis, Amanda F. Francisco, Shiromani Jayawardhana, Harry Langston, Martin C. Taylor, John M. Kelly
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Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/850b2861c2234ed780d6b62cca0fdb24
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spelling oai:doaj.org-article:850b2861c2234ed780d6b62cca0fdb242021-12-02T15:07:44ZImaging the development of chronic Chagas disease after oral transmission10.1038/s41598-018-29564-72045-2322https://doaj.org/article/850b2861c2234ed780d6b62cca0fdb242018-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-29564-7https://doaj.org/toc/2045-2322Abstract 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.Michael D. LewisAmanda F. FranciscoShiromani JayawardhanaHarry LangstonMartin C. TaylorJohn M. KellyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-8 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Michael D. Lewis
Amanda F. Francisco
Shiromani Jayawardhana
Harry Langston
Martin C. Taylor
John M. Kelly
Imaging the development of chronic Chagas disease after oral transmission
description Abstract 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.
format article
author Michael D. Lewis
Amanda F. Francisco
Shiromani Jayawardhana
Harry Langston
Martin C. Taylor
John M. Kelly
author_facet Michael D. Lewis
Amanda F. Francisco
Shiromani Jayawardhana
Harry Langston
Martin C. Taylor
John M. Kelly
author_sort Michael D. Lewis
title Imaging the development of chronic Chagas disease after oral transmission
title_short 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_sort imaging the development of chronic chagas disease after oral transmission
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/850b2861c2234ed780d6b62cca0fdb24
work_keys_str_mv AT michaeldlewis imagingthedevelopmentofchronicchagasdiseaseafteroraltransmission
AT amandaffrancisco imagingthedevelopmentofchronicchagasdiseaseafteroraltransmission
AT shiromanijayawardhana imagingthedevelopmentofchronicchagasdiseaseafteroraltransmission
AT harrylangston imagingthedevelopmentofchronicchagasdiseaseafteroraltransmission
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