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
Schistosoma mansoni infections of CBA/J and C57BL/6 mice provided the hosts with partial protection against reinfection by S. mansoni cercariae. The level of protection, assayed by perfusion 21–25 days after challenge, varied over the course of infection. After patency the degree of resistance observed in CBA/J mice was related to the adult worm burden harbored by the mice. The same was initially true in C57BL/6 mice. Those C57BL/6 mice which lived until a chronic state of infection were rarely well protected and harbored few female worms. Strain differences were also apparent in that the number of worms required by C57BL/6 mice to establish the same level of protection as CBA/J mice was double that needed by CBA/J mice. Measurements were made of the newly formed egg-induced hepatic granulomas throughout the infection period (up to 30 weeks after infection). The data revealed that although the pattern by which C57BL/6 mice developed maximum granuloma formation and subsequent modulation was identical to that observed in CBA/J mice, C57BL/6 granulomas were consistently half the volume of their counterpart lesions in CBA/J mice.