Mouse model for Chagas disease: immunohistochemical distribution of different stages of Trypanosoma cruzi in tissues throughout infection.

J Guarner Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by J Guarner in
Current site
Google Scholar
PubMed Close
,
J Bartlett Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by J Bartlett in
Current site
Google Scholar
PubMed Close
,
S R Zaki Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by S R Zaki in
Current site
Google Scholar
PubMed Close
,
D G Colley Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by D G Colley in
Current site
Google Scholar
PubMed Close
,
M J Grijalva Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by M J Grijalva in
Current site
Google Scholar
PubMed Close
, and
M R Powell Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30341, USA.

Search for other papers by M R Powell in
Current site
Google Scholar
PubMed Close
DOI:
https://doi.org/10.4269/ajtmh.2001.65.152
Volume/Issue:
Volume 65: Issue 2
Page(s):
152–158
Restricted access
Get Permissions

Different stages of Trypanosoma cruzi are seen during mammalian infection. Histologic sections of infected hearts have shown amastigotes and, when using immunohistochemistry (IHC), parasite antigens; however, demonstration of trypomastigotes in these tissues has proven elusive. Using a mouse strain that develops chagasic cardiomyopathy (histologically similar to human infection) 70 days after injecting T. cruzi-Brazil strain, we studied the distribution of parasite stages and the extent of inflammation. All organs had varying amounts of mononuclear inflammation by day 10, which peaked between day 20 and day 30, and decreased by day 50. Amastigotes were detected in myocytes, histiocytes, acinar pancreatic cells, astrocytes and ependymal cells by day 10, and the number of amastigotes peaked on day 30. Immunohistochemistry demonstrated trypomastigotes in sinusoids, vessels and interstitial tissues of several organs between day 15 and 50. Abundant parasite antigens (granular staining) were detected in connective tissues throughout the infection. The burden of amastigotes and trypomastigotes during the acute phase seems to correlate with the degree of inflammation and granular staining in the chronic stage.

Author Notes

Published Online:
Aug 2001
Cover The American Journal of Tropical Medicine and Hygiene
The American Journal of Tropical Medicine and Hygiene
Print ISSN:
0002-9637
Past two years Past Year Past 30 Days
Abstract Views 4153 4036 47
Full Text Views 422 17 0
PDF Downloads 211 14 0
 

 

 

 
 
Affiliate Membership Banner
 
 
Research for Health Information Banner
 
 
CLOCKSS
 
 
 
Society Publishers Coalition Banner
Save