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
Dr. McGhee has presented experimental evidence that ducklings infected with Plasmodium lophurae and given sub-curative quinine treatment suffer from an anemia that differs from the anemias resulting from simple blood loss, or from infection with P. relictum. In this anemia the radical reduction of polychromatophil erythroblasts seemed to be associated with the loss of this cell in the bone marrow. In discussing possible causative mechanisms for this anemia, it was suggested that these cellular elements might have been destroyed by an auto-immune process.
The implication here is that the association of host cell, parasite, and drug form an antigen complex that will sensitize ducklings and that the resulting antibodies react with and incapacitate, or destroy the erythroblast tissues of marrow. It would be of interest to determine whether or not a similar anemia would result in normal ducklings following passive transplant of humoral or cellular elements from P. lophurae-infected and quinine-treated ducklings, after artificial blood loss, which would normally make erythroblasts evident in the peripheral blood of the recipient animals.
Department of Microbiology and Immunology, State University of New York, College of Medicine, Brooklyn, New York.