Proliferative Glomerulonephritis, Hypocomplementemia, and Nucleic Acid Antibodies in Rats Infected with Trypanosoma Rhodesiense

Herbert B. LindsleyDepartment of Medicine, University of Kansas Medical Center, Department of Pathology, University of Arizona Health Science Center, Kansas City, Kansas 66103

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Raymond B. NagleDepartment of Medicine, University of Kansas Medical Center, Department of Pathology, University of Arizona Health Science Center, Kansas City, Kansas 66103

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Daniel J. StechschulteDepartment of Medicine, University of Kansas Medical Center, Department of Pathology, University of Arizona Health Science Center, Kansas City, Kansas 66103

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Host immunologic responses were studied in Sprague-Dawley rats infected with a human isolate of Trypanosoma Rhodesiense. retro-orbital sinus bleedings were obtained on days 0 and 14 and at 21 or 28 days. Infected and control rats were sacrified on day 21 or 28 of the infection. Mild glomerulitis, as assessed by increased cellularity and/or widening of the mesangial region, was apparent in 6 of 7 infected animals. Finely granular deposits of IgM and IgGl were found in most glomeruli with less prominent deposits of IgGa and IgA. Focal cortical mononuclear interstitial infiltrates were present in 2 of 7 rats. Subepithelial or mesangial electron dense deposits were present in the glomeruli of infected rats. Hypocomplementemia was present by day 21 and involved both the classical and alternative pathways of complement activation. Antibodies to native DNA and single-stranded RNA were present by day 21. These studies indicate the feasibility of studying trypanosomal glomerulonephritis in rats and will provide a convenient model for detailed immunologic and morphologic investigation of host immune responses in African trypanosomiasis.

Author Notes

Department of Pathology, University of Arizona Health Science Center, Tucson, Arizona 85724.

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