Infection with different Trypanosoma cruzi populations in rats: myocarditis, cardiac sympathetic denervation, and involvement of digestive organs

Am J Trop Med Hyg. 2000 May;62(5):604-12. doi: 10.4269/ajtmh.2000.62.604.

Abstract

We tested four isolates of Trypanosoma cruzi to assess parasite virulence and ability to cause myocarditis, cardiac sympathetic denervation, and histopathologic alterations in organs of the digestive system. The susceptibility of rats depends on the population of T. cruzi, with the ABC strain and the CL-Brener clone killing all animals, regardless of the parasitemic pattern. All tested T. cruzi populations caused acute myocarditis, but failed to induce histologic alterations in the intestine. The Cl-Brener and ABC isolates caused esophageal myositis. The myocarditis caused by the ABC, CL-Brener, and Y isolates was severe, but resolution started at the end of the acute phase. In contrast, the Col 1.7 G2 clone induced mild and sustained myocarditis. Our results also showed that T. cruzi populations able to induce severe acute myocarditis caused marked sympathetic denervation, but recovery of normal cardiac histology and innervation occurred. The sustained myocarditis induced by Col 1.7 G2 clone failed to cause sustained denervation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chagas Cardiomyopathy / parasitology*
  • Chagas Cardiomyopathy / pathology
  • Chagas Cardiomyopathy / physiopathology
  • Chagas Disease / parasitology*
  • Chagas Disease / pathology
  • Chagas Disease / physiopathology
  • Digestive System Diseases / parasitology*
  • Digestive System Diseases / pathology
  • Esophagus / parasitology
  • Esophagus / pathology
  • Female
  • Heart / innervation*
  • Heart / parasitology
  • Intestinal Diseases, Parasitic / parasitology
  • Intestinal Diseases, Parasitic / pathology
  • Intestines / parasitology
  • Intestines / pathology
  • Male
  • Rats
  • Sympathectomy*
  • Trypanosoma cruzi / classification
  • Trypanosoma cruzi / pathogenicity*