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Updated: Feb 7, 2026

Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
Published on: July 29, 2012
Imaging the development of chronic Chagas disease after oral transmission
Michael D Lewis1, Amanda F Francisco2, Shiromani Jayawardhana2
1Department of Pathogen Molecular Biology, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT, United Kingdom. michael.lewis@lshtm.ac.uk.
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.
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