Trypanosoma cruzi infection and the rat central nervous system: proliferation of parasites in astrocytes and the brain reaction to parasitism

Chagas’ disease, caused by the protozoan Trypanosoma cruzi, is characterized by an acute phase in which parasites circulate in the blood and proliferate in several cell types, especially muscle cells. A life-long chronic phase follows the acute phase. In young patients, the acute phase is more sever...

Full description

Saved in:

Bibliographic Details
Published in:	Brain research bulletin Vol. 53; no. 2; pp. 153 - 162
Main Authors:	Da, João R, Camargos, MataElizabeth R.S, Chiari, Egler, Machado, Conceição R.S
Format:	Journal Article
Language:	English
Published:	New York, NY Elsevier Inc 15-09-2000 Elsevier Science
Subjects:	Age Factors Animals Animals, Newborn - parasitology Astrocytes Astrocytes - parasitology Astrocytes - pathology Astrocytes - ultrastructure Biological and medical sciences Brain Brain - parasitology Brain - pathology Brain - ultrastructure Cell Count Cell Division - physiology Chagas Disease - parasitology Chagas Disease - pathology Chagas’ disease Experimental protozoal diseases and models Glial nodules Host-Parasite Interactions - physiology Infectious diseases Macrophages Macrophages - parasitology Macrophages - pathology Macrophages - ultrastructure Male Medical sciences Microglia Microglia - parasitology Microglia - pathology Microglia - ultrastructure Neurons - parasitology Neurons - pathology Neurons - ultrastructure Neutrophils Neutrophils - parasitology Neutrophils - pathology Neutrophils - ultrastructure Parasitemia - parasitology Parasitemia - physiopathology Parasitic diseases Protozoal diseases Rats Rats, Sprague-Dawley Time Factors Trypanosoma cruzi Trypanosoma cruzi - parasitology Trypanosoma cruzi - physiology Trypanosoma cruzi - ultrastructure Brain Astrocytes Chagas’ disease Neutrophils Glial nodules Macrophages Microglia Kinetoplastida Protozoa Protozoal disease Rat Neuroglia Rodentia Central nervous system Chagas disease Parasitosis Astrocyte Proliferation Trypanosoma cruzi Infection Vertebrata Mammalia Animal Parasitism Trypanosomiasis Brain (vertebrata)
Online Access:	Get full text
Tags:	Add Tag No Tags, Be the first to tag this record!

Description
Summary:	Chagas’ disease, caused by the protozoan Trypanosoma cruzi, is characterized by an acute phase in which parasites circulate in the blood and proliferate in several cell types, especially muscle cells. A life-long chronic phase follows the acute phase. In young patients, the acute phase is more severe, and meningoencephalitis frequently occurs in children before 2 years of age. Parasites have been rarely observed in neurons but their presence inside glial cells has been reported without characterization of the glial cell type. The cells involved in the brain reaction to the parasites and the time course of this reaction remain to be studied. Therefore, using suckling and juvenile rats and different T. cruzi populations, we aimed at determining the brain target for parasite proliferation and the cells involved in the brain reaction. Around the middle of the acute phase, histological and ultrastructural findings indicated that T. cruzi proliferates in astrocytes, forming nests devoid of enclosing membrane as described for non-glial cells. The brain nodular reaction comprised astrocytes, microglia, macrophages and neutrophils. Resting microglia was devoid of parasites in contrast to macrophages and neutrophils that probably participate in parasite removal. Suckling animals were significantly more affected, the numbers of nests and nodules varying with inoculum size. Histoquantitative analysis showed higher number of nests at the parasitemic peak (day 13) and drastic fall at day 20 post-inoculation. The highest number of nodules occurred at day 20 with drastic reduction at day 30. Recovery from histopathological alterations occurred even in surviving younger animals.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	0361-9230 1873-2747
DOI:	10.1016/S0361-9230(00)00326-9