By H. J. Bensted, W. Bulloch, L. Dudgeon, A. G. Gardner, E. D. W. Greig, D. Harvey, W. F. Harvey, T. J. Mackie, R. A. O'Brien, H. M. Perry, H. Scutze, P. Bruce White, W. J. Wilson. London, 1929. His Majesty's Stationery Office. Pp. 1–482
by A. Trevor Willis, M.D., B.S. (Melb.), Ph.D. (Leeds), M.C.Path., M.C.P.A., Reader in Microbiology, Monash University, formerly Lecturer in Bacteriology, University of Leeds. xiv + 234 pages, illustrated, second edition. Butterworth Inc., Washington. 1965. $8.50
Twelve beagles were infected with 200 Dirofilaria immitis infective larvae to study glomerular lesions associated with filariasis. All developed high serum levels of antibodies to dirofilarial antigens and became persistently microfilaremic. The dogs were killed at various times between 398 and 562 days post-infection and renal lesions were examined by light, electron, and immunofluorescent microscopy and antibody elution techniques. A membranoproliferative glomerulonephritis was observed in all dogs. Immunofluorescence was positive in all; predominantly in a fine granular pattern along the glomerular capillary wall. Ultrastructural examination showed intramembranous globular electron-dense deposits and a linear band of fine electron-dense particles in all dogs. Antibody elution studies demonstrated antibody reactive to dirofilarial antigens.
In a subsequent experiment, an aqueous-soluble antigen prepared from adult female D. immitis was infused into the renal arteries of 5 heartworm-naive dogs. Immunofluorescent examination of the infused kidneys showed dirofilarial antigen present on the glomerular capillary wall in a fine granular pattern indicating there was adherence of the antigen to the capillary wall. These observations support the hypothesis of in situ immune complex formation as part of the pathogenesis of glomerulonephritis associated with dirofilariasis.