Trypanosoma cruzi infection: do distinct populations cause intestinal motility alteration?

Chagas disease, caused by Trypanosoma cruzi, is an important public health problem in Latin America. Disturbances in gastrointestinal motility are observed in 15-20% of patients at the chronic phase. We previously observed a decrease in intestinal motility in mice infected with Y strain from T. cruzi. Thus, we decided to test if infection with other T. cruzi strains also caused the intestinal disturbance. Male adult Swiss mice were infected intraperitoneally with CL-Brener clone (CL-B), Brazil strain (Br), or Dm28 clone (Dm) of T. cruzi. All infected mice presented a low cumulative mortality (CL-B, 17%; Br, 8%; Dm, 25%) at 35 days post infection (dpi) and their typical parasitemia curves. Br and Dm groups exhibited a maximal reduction of intestinal motility at 35 dpi (176.8 +/- 51.3 and 198.3 +/- 52.6 min, respectively), when compared with non-infected mice (90.2 +/- 19.5 min). However, CL mice presented the peak of delayed intestinal transit at 12 dpi (191.0 +/- 33.3 min), when compared with non-infected mice (105.6 +/- 26.4 min), very close to the 15 dpi for the intense alteration (310.2 +/- 67.4 min) observed with the Y strain. We clearly demonstrate a reduction in intestinal motility in mice infected with different groups of T. cruzi during the acute phase of the infection. Since Br, Dm, and CL strains presented low mortality rates in adult Swiss mice, a prospective study concerning the chronic intestinal alteration is encouraged, particularly for studies of alternative therapies.

Applicability of the use of charcoal for the evaluation of intestinal motility in a murine model of Trypanosoma cruzi infection.

Chagas disease, caused by the protozoan Trypanosoma cruzi, remains a serious public health problem in Latin America. In relation to digestive problems, 4.5% of patients show mega syndromes (megacolon) in the chronic phase. In this article, we evaluated intestinal motility at the acute phase of T. cruzi infection through charcoal ingestion in adult mice. After infection, Swiss mice were administered an aqueous suspension of charcoal in water by gavage. Decrease in intestinal motility was determined by increased time of appearance of charcoal in the feces. The uninfected group showed a mean time of charcoal elimination of 109.0 +/- 14.6 min throughout the assay. On the other hand, infected mice presented a significant increase in charcoal defecation time during infection. At 15 days postinfection, infected mice showed a significant increase in charcoal defecation time, 310.2 +/- 67.4 min when compared to the uninfected group, which presented 97.8 +/- 31.8 min, indicating that the T. cruzi infection interferes with intestinal motility. Our results demonstrate that the use of charcoal is an ethical and efficient procedure to evaluate the intestinal motility in the murine model of T. cruzi infection.