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

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.

[1]  M. Blennerhassett,et al.  Early damage of sympathetic neurons after co‐culture with macrophages: a model of neuronal injury in vitro , 2000, Neuroreport.

[2]  C. Machado,et al.  Cardiac autonomic denervation in congestive heart failure: comparison of Chagas' heart disease with other dilated cardiomyopathy. , 2000, Human pathology.

[3]  S. Zucoloto,et al.  Nitric oxide is involved in the lesions of the peripheral autonomic neurons observed in the acute phase of experimental Trypanosoma cruzi infection. , 1999, Experimental parasitology.

[4]  R. Gazzinelli,et al.  Platelet-Activating Factor Induces Nitric Oxide Synthesis in Trypanosoma cruzi-Infected Macrophages and Mediates Resistance to Parasite Infection in Mice , 1999, Infection and Immunity.

[5]  S. D. Pena,et al.  Differential tissue distribution of diverse clones of Trypanosoma cruzi in infected mice. , 1999, Molecular and biochemical parasitology.

[6]  S. Morris,et al.  Expression of cardiac cytokines and inducible form of nitric oxide synthase (NOS2) in Trypanosoma cruzi-infected mice. , 1999, Journal of molecular and cellular cardiology.

[7]  R. C. Melo,et al.  Depletion of radiosensitive leukocytes exacerbates the heart sympathetic denervation and parasitism in experimental Chagas' disease in rats , 1998, Journal of Neuroimmunology.

[8]  E. Read,et al.  Seroepidemiology of Trypanosoma cruzi, etiologic agent of Chagas' disease, in US blood donors. , 1997, The Journal of infectious diseases.

[9]  R. Tarleton,et al.  "Autoimmune rejection" of neonatal heart transplants in experimental Chagas disease is a parasite-specific response to infected host tissue. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[10]  M. Tibayrenc,et al.  Impact of clonal evolution on the biological diversity of Trypanosoma cruzi , 1997, Parasitology.

[11]  L V Kirchhoff,et al.  American Trypanosomiasis (Chagas Disease) , 2018, Red Book (2018).

[12]  D. Troyer,et al.  Induction of proinflammatory cytokine expression in experimental acute Chagasic cardiomyopathy. , 1996, Biochemical and biophysical research communications.

[13]  C. Machado,et al.  Preganglionic fibres of the adrenal medulla and cervical sympathetic ganglia: differential involvement during experimental American trypanosomiasis in rats , 1996, International journal of experimental pathology.

[14]  E. Castaños-Vélez,et al.  Role of nitric oxide in resistance and histopathology during experimental infection with Trypanosoma cruzi. , 1995, Immunology letters.

[15]  F. Cunha,et al.  Nitric oxide is involved in control of Trypanosoma cruzi-induced parasitemia and directly kills the parasite in vitro , 1994, Infection and immunity.

[16]  R. Tarleton,et al.  Depletion of T-cell subpopulations results in exacerbation of myocarditis and parasitism in experimental Chagas' disease , 1994, Infection and immunity.

[17]  T. Kipnis,et al.  A critical evaluation of the expression of parasitemia in experimental Chagas' disease. , 1993, Revista do Instituto de Medicina Tropical de Sao Paulo.

[18]  C. Vnencak-Jones,et al.  Amplification of a Trypanosoma cruzi DNA sequence from inflammatory lesions in human chagasic cardiomyopathy. , 1993, The American journal of tropical medicine and hygiene.

[19]  J. Dvorak,et al.  Identification, isolation, and characterization of naturally-occurring Trypanosoma cruzi variants. , 1993, Molecular and biochemical parasitology.

[20]  R. Tarleton,et al.  Predominance of CD8+ T lymphocytes in the inflammatory lesions of mice with acute Trypanosoma cruzi infection. , 1993, The American journal of tropical medicine and hygiene.

[21]  R. Kaneno,et al.  CD8+ cells and natural cytotoxic activity among spleen, blood, and heart lymphocytes during the acute phase of Trypanosoma cruzi infection in rats , 1992, Infection and immunity.

[22]  S. G. Andrade.  Influence of Trypanosoma cruzi strain on the pathogenesis of chronic myocardiopathy in mice. , 1990, Memorias do Instituto Oswaldo Cruz.

[23]  C. Machado,et al.  Experimental American trypanomiasis in rats: sympathetic denervation, parasitism and inflammatory process. , 1989, Memorias do Instituto Oswaldo Cruz.

[24]  C. Machado,et al.  Changes in choline acetyltransferase activity of rat tissues during Chagas' disease. , 1987, Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas.

[25]  R. Isturiz,et al.  Chagas Disease , 2021, Neglected Tropical Diseases.

[26]  J. S. Oliveira.  A natural human model of intrinsic heart nervous system denervation: Chagas' cardiopathy. , 1985, American heart journal.

[27]  C. Machado,et al.  Recovery from heart norepinephrine depletion in experimental Chagas' disease. , 1978, The American journal of tropical medicine and hygiene.

[28]  J. Scorza,et al.  Acute myocarditis in rats inoculated with Trypanosoma cruzi: study of animals sacrificed between the fourth and twenty-ninth day after infection. , 1972, Revista do Instituto de Medicina Tropical de Sao Paulo.

[29]  F. Köberle.  Chagas' disease and Chagas' syndromes: the pathology of American trypanosomiasis. , 1968, Advances in parasitology.

[30]  W. Abelmann,et al.  CHRONIC AND PROGRESSIVE MYOCARDITIS AND MYOSITIS IN C3H MICE INFECTED WITH TRYPANOSOMA CRUZI. , 1964, The American journal of tropical medicine and hygiene.

[31]  Z. Brener.  Therapeutic activity and criterion of cure on mice experimentally infected with Trypanosoma cruzi. , 1962, Revista do Instituto de Medicina Tropical de Sao Paulo.

[32]  M. Kolodny.  STUDIES ON AGE RESISTANCE AGAINST TRYPANOSOME INFECTIONS: I. THE RESISTANCE OF RATS OF DIFFERENT AGES TO INFECTION WITH TRYPANOSOMA CRUZI , 1939 .