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.
Highlights
Chagas disease (American trypanosomiasis) is caused by infection with Trypanosoma cruzi, a protozoan parasite
The oral route is important because consumption of triatomines by wild mammals is a key part of natural T. cruzi transmission cycles[17]
Trypanosoma cruzi is unusual, though not unique, amongst protozoan parasites in its ability to establish a systemic infection in its host after transmission via an oral route[27]
Summary
Chagas disease (American trypanosomiasis) is caused by infection with Trypanosoma cruzi, a protozoan parasite. After several rounds of replication, amastigotes make a developmental transition resulting in bloodstream trypomastigotes (BTs), which can either invade a new host cell, or complete the life cycle by transforming into epimastigotes if they are taken up by a triatomine bug as part of a blood meal. The number of acute Chagas disease cases attributed to oral infection has increased dramatically since 20001,16 It is not clear whether this trend reflects better surveillance or genuine changes in transmission patterns driven by eco-epidemiological factors. Experimental studies have reproduced features of severe acute Chagas disease in mice after oral inoculation[20,21] It is not known whether reports of increased severity of orally-acquired infections can be explained by the route of parasite entry or other co-varying factors.
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