AJTMH Tropical Medicine and Hygiene News
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am. J. Trop. Med. Hyg., 13(2), 1964, pp. 272-280
Copyright © 1964 by The American Society of Tropical Medicine and Hygiene

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Federici, E. E.
Right arrow Articles by Neva, F. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Federici, E. E.
Right arrow Articles by Neva, F. A.

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

Ernest E. Federici{dagger}, Walter H. Abelmann{ddagger} AND 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

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.


* Supported in part by Training Grant HTS 5254 from the National Heart Institute, National Institutes of Health, U. S. Public Health Service, and in part by U.S.P.H.S. Training Grant 2E-177 for the Harvard Training Program in Tropical Medicine.


{dagger} 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.


{ddagger} 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.




This article has been cited by other articles:


Home page
Infect. Immun.Home page
J. L. Hardison, R. A. Wrightsman, P. M. Carpenter, T. E. Lane, and J. E. Manning
The Chemokines CXCL9 and CXCL10 Promote a Protective Immune Response but Do Not Contribute to Cardiac Inflammation following Infection with Trypanosoma cruzi
Infect. Immun., January 1, 2006; 74(1): 125 - 134.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
J. L. Hardison, R. A. Wrightsman, P. M. Carpenter, W. A. Kuziel, T. E. Lane, and J. E. Manning
The CC Chemokine Receptor 5 Is Important in Control of Parasite Replication and Acute Cardiac Inflammation following Infection with Trypanosoma cruzi
Infect. Immun., January 1, 2006; 74(1): 135 - 143.
[Abstract] [Full Text] [PDF]


Home page
CirculationHome page
A. P. M.P. Marino, A. da Silva, P. dos Santos, L. M. d. O. Pinto, R. T. Gazzinelli, M. M. Teixeira, and J. Lannes-Vieira
Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES) Antagonist (Met-RANTES) Controls the Early Phase of Trypanosoma cruzi-Elicited Myocarditis
Circulation, September 14, 2004; 110(11): 1443 - 1449.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1964 by the American Society of Tropical Medicine and Hygiene.