Chronic and Progressive Myocarditis and Myositis in C3H Mice Infected with Trypanosoma Cruzi*

Ernest E. Federici Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Department of Medicine, Harvard Medical School, and Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts

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Walter H. Abelmann Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Department of Medicine, Harvard Medical School, and Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts

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Franklin A. Neva Thorndike Memorial Laboratory and the Second and Fourth (Harvard) Medical Services, Boston City Hospital, Department of Medicine, Harvard Medical School, and Department of Tropical Public Health, Harvard School of Public Health, Boston, Massachusetts

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Summary

A study of the clinical and pathological course of experimental myotropic Chagas' disease in the mouse is reported. Forty-nine C3H mice, 3 to 5 weeks of age, were inoculated with a Colombian strain of Trypanosoma cruzi. Observations of body weight, spontaneous activity, parasite counts and histopathology were made up to 388 days following inoculation.

The disease was characterized by a benign parasitemic stage, followed by a chronic progressive myocarditis and myositis. During the first 2 months after the inoculation, infected animals could not be differentiated in appearance and body weight from control animals. Parasitemia reached a maximum at the end of the first month and subsided at the end of the second month. Gross pathologic examination during this stage of the infection showed consistent splenomegaly. The mean heart weight of infected animals did not differ significantly from that of the controls. Microscopic study revealed moderate infiltration of cardiac and skeletal muscle and occasional intracellular T. cruzi.

In the third month, the infected animals began to show ruffled fur, spotty alopecia, and progressive weight loss. In time, the infected animals appeared more ill, and deaths occurred. Spontaneous activity, measured from the fifth through the eighth month of infection, was consistently and progressively lower in the infected animals than in the controls. Gross pathologic examination in these later stages of the disease frequently revealed muscle wasting and cardiac enlargement. Between the sixth and the thirteenth month mean heart weight in relation to body weight in infected animals was significantly greater than in control animals. Microscopic study revealed continued and increasing involvement of cardiac muscle. Intracellular organisms were irregularly present in cardiac muscle to day 388.

Author Notes

Research Fellow, Massachusetts Heart Association. Formerly Research Fellow, Thorndike Memorial Laboratory, Boston City Hospital, and the Department of Medicine, Harvard Medical School. Present address: St. Elizabeth's Hospital, Elizabeth, New Jersey.

Assistant Professor of Medicine, Harvard Medical School; Assistant Physician, Thorndike Memorial Laboratory, Boston City Hospital; Assistant Cardiologist, Children's Hospital Medical Center, Boston, Massachusetts.

Associate Professor of Tropical Public Health, Harvard School of Public Health; Clinical Associate in Medicine, Harvard Medical Unit, Boston City Hospital, Boston, Massachusetts.

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