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.

Acute Trypanosoma cruzi experimental infection induced renal ischemic/reperfusion lesion in mice.

Experimental acute infection with Trypanosoma cruzi in mice promotes an intense myocarditis and other systemic changes. However, the network of pathophysiological disorders and renal injury caused by the infection has not been elucidated. Our previous results with a murine model observed a discrete acute myocarditis and high mortality with significant inflammatory kidney injury with T. cruzi infection. The aim of this study was to investigate the mechanisms of kidney injury caused by the parasite in mice during the experimental acute phase. Results employing BALB/c mice infected with T. cruzi of Y strain showed renal injury on the 6th day postinfection (dpi) caused by a transitory decrease of renal blood flow. Acute kidney injury (AKI) was also observed similar to the model of ischemia/reperfusion lesion in these infected mice. The injury was not related to the presence (or multiplication) of parasites. Only rare nests were microscopically detected, and the presence of scattered parasites in renal parenchyma was seen on the 15th dpi. Thus, it was observed that during the acute phase of the disease, AKI in infected mice is linked to early cardiovascular effects, including heart failure, caused by striking inflammatory lesions in the myocardium, which lead to the high mortality rate of animals.