Renal Disease in Chronic Experimental Trypanosoma Gambiense Infections

Eric A. E. Van MarckDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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Andree BeckersDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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Andre M. DeelderDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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Wim JacobDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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Marc WeryDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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Paul L. J. GigaseDepartments of Pathology and Protozoology, Prince Leopold Institute of Tropical Medicine, State University Leiden, Department of Parasitology, Universitaire Instelling Antwerpen, Laboratory of Electron Microscopy, Antwerp, Belgium

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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 7–22 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 9–15 weeks developed morphologically similar glomerular lesions. Four other trypanosome stocks did not evoke renal alterations in 17 other rats infected for 13–56 weeks. Experimental infection in mice or rats appears to be a suitable model for the study of renal disease in chronic African sleeping sickness.

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