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
Overt hepatosplenic schistosomiasis developed in mice after their exposure to cercariae of Schistosoma mansoni. After 8, 11, 33, and 52 weeks of infection, livers of the mice were prepared for light and electron-microscopic study. At all intervals, randomly observed and periportal parenchymal cells exhibited ultrastructural integrity. In the early phase of the disease, paragranuloma hepatocytes displayed subcellular alterations indicative of hepatocellular injury, but, at the late intervals, paragranuloma hepatocytes revealed no major ultrastructural abnormality.
These observations provided further evidence that toxic factors from adult schistosome worms do not adversely affect the hepatic parenchyma. Rather, the ultrastructural data corroborated previous evidence, indicating that the schistosome ovum is the primary factor in the pathogenesis of overt hepatosplenic schistosomiasis mansoni.
The electron-microscopic study revealed the schistosome pigment as comprised of intensely osmiophilic, very dense, ovoid and doughnut-shaped structures, which were confined in phagosomes. In this form, the pigment was observed in Kupffer's cells along the hepatic sinusoids and in the phagocytic cells of the hepatic granulomata.