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
This study characterizes a Plasmodium berghei white rat model of P. falciparum malaria in the pregnant human. Seventy-day-old and 114-day-old female rats, given an infecting inoculum at time of mating, had higher parasitemias and a more severe anemia than age- and sex-matched controls. Under these experimental conditions, the parasitemia went to crisis in all animals and there were no fatal infections. In contrast, all animals died when the infection was initiated 7 days after conception, a timing that brought a coincidence of peak parasitemia and term. Pregnancy during the post-crisis subpatent period did not cause recrudescence. At the time of delivery, the parasitemia was consistently higher in the placental (crush smear) blood than in the peripheral (tail) blood. This difference was greatest in animals giving birth shortly before or 1–2 days after the parasitemic crisis. Very young, compact parasite forms predominated in the placental blood, whereas trophozoites predominated in the peripheral blood.