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Two recently isolated stocks of Trypanosoma brucei gambiense of human origin gave rise to a moderate to severe proliferative or membranoproliferative glomerulonephritis in 40 or 44 NMRI and C57BL/6J mice infected for 722 weeks. Extensive granular deposits of C3, IgG1 and IgG3 were found in the mesangium, together with smaller quantities of IgG2a, IgG2b, and IgM. No trypanosomal antigen could be detected in the deposits though specific anti-trypanosoma antibodies were found in kidney eluates. By electron microscopy, a conspicuous proliferation of mesangial and endothelial cells was observed and electrondense deposits were seen in a mesangial and subepithelial localization. With one of these trypanosome stocks, four of seven Wistar rats infected for 915 weeks developed morphologically similar glomerular lesions. Four other trypanosome stocks did not evoke renal alterations in 17 other rats infected for 1356 weeks. Experimental infection in mice or rats appears to be a suitable model for the study of renal disease in chronic African sleeping sickness.
Accepted for publication December 6, 1980.
Address reprint requests to: Dr. E. A. E. Van Marck, Prince Leopold Institute of Tropical Medicine, Department of Pathology, Nationalestraat 155, B-2000 Antwerp, Belgium.
* An abstract of this work has been published in the Abstract Book of the 4th International Congress of Immunology (of the International Union of Immunological Societies IUIS), Paris, July 2126, 1980.
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