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
The course of an infection with the BEV strain of Toxoplasma gondii was observed in splenectomized mice, and in mice treated with cortisone and 6-MP—procedures known to modify or suppress the normal immune response. It was observed that the pathogenesis of the disease was greatly altered in the experimental animals, being distinguished by signs of severe neurological involvement, and by the eventual death of most of the mice from a disseminated toxoplasmic meningoencephalitis. Signs of the disease were ruffled fur, shuddering, weakness of limbs, diarrhea, head-tilting, choreiform movements, arched spine and sinuous rolling motions, posterior paraplegia, emaciation, coma, and death. Also observed were persistence of trophozoites in peritoneal exudate, earlier appearance and greater numbers of cysts in the brain, development of many cysts in large clusters, and widespread inflammation of the brain and meninges.
Challenge of the survivors of the four groups of experimental mice with the virulent RH strain after 1 month of primary infection indicated that immunity had developed to a lesser degree in the treated mice. It is hypothesized that as a direct consequence of the immuno-suppression, there was continuous parasite proliferation in tissues and hematogenous transport of trophozoites to the brain.
Postdoctoral Research Fellow, U. S. National Institute of Allergy and Infectious Diseases.