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
In three experiments it was shown that mice that had recovered from P. chabaudi infection were resistant to challenging B. rodhaini infections. Mice that were challenged 1 week after recovery appeared to be more resistant than those challenged after 5 weeks. On the other hand, mice recovered from P. chabaudi appeared to be as susceptible as control mice when they were challenged with P. berghei. There was, however, in each of three experiments a 2- to 3-day delay in the development of P. berghei parasitemia in the mice recovered from infection with P. chabaudi.
In two experiments it was evident that rats that had recovered from P. berghei infection were resistant to challenge with B. rodhaini. Resistance of rats in the converse situation is less clear since the resistance of rats recovered from infection with B. rodhaini was obscured by extremely high P. berghei parasitemia in three of 10 recovered rats.
The results of these experiments suggest that part of the immunizing mechanisms in both malaria and babesiosis are nonspecific and that the same mechanism probably pertains in both infections. It is suggested that the serum antigens in acute infections, which have been shown to be both nonspecific and immunogenic in previous work, are primarily responsible for the observed results.
The fact that mice that had recovered from P. chabaudi infection resisted B. rodhaini, but did not resist with P. berghei does not indicate that P. berghei is a more virulent parasite. In our experience B. rodhaini is as lethal for mice as is P. berghei. We believe that the apparent lack of resistance of these mice to P. berghei is a manifestation other mechanisms, that is, the selection of “immunity-resistant” variants or mutants by the immunized mice.