Orally Acquired Chagas Disease in Rats Exposed to Naturally Infected Triatominae Bugs.

Chagas disease, also known as American Trypanosomiasis, is a parasitic infectious disease that is primarily transmitted by infected kissing bugs belonging to the subfamily Triatominae. Military personnel that conduct deployment operations (field training, patrols, combat, physical training and sustainment) in kissing-bug infested habitats are at risk. Transmission of disease to humans occurs by contact of skin and mucous membranes with infected kissing bug's feces. Additionally, transmission can result from blood transfusion, and ingestion of infected insects. However, the exact route of infection for military personnel (including military working dogs) remains elucidated. In this laboratory study, Trypanosoma cruzi-infected triatomine bugs collected from the field were used to evaluate various oral exposures in rats. Treatment groups included: 1) ingestion of T. cruzi-positive insect excreta; 2) ingestion of T. cruzi-infected insect digestive tract; 3) oral exposure via mucosal scraping; and 4) ingestion of a live infected kissing bug. Rats were monitored for 12 weeks. An indirect immunofluorescent assay to detect parasite-specific immunoglobulin (Ig) M and IgG was used to estimate the rate of infection. At necropsy, heart, spleen, kidney, and stomach were collected to assess histopathology. Trypanosoma cruzi infection was established through various oral exposures. This resulted in the development of anti-T. cruzi antibodies. Rats exposed via ingestion of whole insect or oral mucosa were comparable to the positive control group in that 86% and 100%, respectively, of animals developed a T. cruzi-specific IgM response by 14 days post infection (dpi). By 21 dpi, a significant number of rats that ingested T. cruzi-infected insect digestive tract (100%) or T. cruzi-positive insect excreta (57%) had developed a parasite-specific IgM response. Amongst all groups receiving oral exposures, a significant number of rats (85.7%) exhibited a T. cruzi-specific IgG response by 35 dpi. We identified a few histopathological differences between groups; nonetheless, we did not observe a consistent statistical trend that would suggest that the histopathology of an oral exposure group was markedly different from another. Collectively, these data suggested that the rate of infection was notably higher than other studies using similar administration routes. As laboratory-raised organisms may not retain the same virulence factors, that data generated in this study may be a better representative of transmission rates occurring naturally. Nonetheless, valuable data is expected to emerge from future studies that assess host susceptibility factors and the vehicle of exposure.