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
Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Division of Veterinary Medical Research, Bureau of Veterinary Medicine, Food and Drug Administration, Bethesda, Maryland 20205
Antimicrofilarial immunity was studied in Dirofilaria immitis-infected doges in order to better understand amicrofilaremic filariasis in man. Sera from dogs with amicrofilaremic infections contained IgG antibodies specific for microfilarial surface antigens detectable by immunofluorescence and in vitro leukocyte adherence. In vivo immune mechanisms were studied by injecting 51Cr-labeled microfilariae (MF) into infected and uninfected dogs. Injected MF were concentrated in lung, liver, spleen, and kidneys of normal and microfilaremic dogs, but circulated throughout the 5-hour study period. In contrast, injected MF were rapidly cleared (15–30 min) from the blood of amicrofilaremic-infected dogs. Tissue radioactivity and histopathology indicated that injected MF were trapped and destroyed in the lungs of these dogs. Antibody-dependent clearance and destruction of MF is a potent antihelminth effector mechanism in canine dirofilariasis. Similar events are likely to occur in amicrofilaremic filariasis in humans.