Abstract

The only existing preventive measure against American trypanosomosis, or Chagas disease, is the control of the transmitting insect, which has only been effective in a few South American regions. Currently, there is no vaccine available to prevent this disease. Here, we present the clinical and cardiac levels of protection induced by expression to Trypanosoma cruzi genes encoding the TcSP and TcSSP4 proteins in the canine model. Physical examination, diagnostic chagasic serology, and serial electrocardiograms were performed before and after immunization, as well as after experimental infection. We found that immunization with recombinant plasmids prevented hyperthermia in the acute phase of experimental infection and produced lymphadenomegaly as an immunological response against the parasite and additionally prevented heart rate elevation (tachycardia) in the acute and/or chronic stages of infection. Immunization with T. cruzi genes encoding the TcSP and TcSSP4 antigens diminished the quality and quantity of the electrocardiographic abnormalities, thereby avoiding progression to more severe developments such as right bundle branch block or ventricular premature complexes in a greater number of dogs.

Highlights

  • Chagas disease (CD) is endemic to the American continent, and 25 million people are at risk in Latin America [1]

  • The TcSP protein expression in the eukaryotic system was determined by immunoblotting, detecting its presence only at 24 and 48 h post transfection with plasmid plasmid containing the TcSP gene (pBCSP) (Figures 1c, and 1d). These results demonstrate that the TcSSP4 and TcSP genes were correctly subcloned into the pBK-CMV vector and that the recombinant plasmids are capable of expression in eukaryotic cells

  • Diagnosis of CD in dogs All of the experimental animals were negative for the chagasic serology test at t1 and were in excellent health, which confirmed the absence of CD before any manipulation

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Summary

Introduction

Chagas disease (CD) is endemic to the American continent, and 25 million people are at risk in Latin America [1]. A major stumbling block for research efforts striving to elucidate the mechanisms of acute and chronic CD pathogenesis is the lack of a suitable animal model. It has been shown that dogs develop diffuse chronic myocarditis with histological and electrocardiographic changes that are found in humans [8,9,10,11,12]; this animal represents a useful experimental model that is gaining attention in the CD research field. The clinical signs in Chagas-infected dogs during both the chronic and acute stages closely resemble the symptoms of human disease [13,14,15]

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