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
1 Clinical Immunology Laboratory, Department of Pathology, Faculty of Medicine, Ramathibodi Hospital, Bangkok, Thailand, and Rajaprachasamasai Institute, Department of Health, Phrapradang, Samutprakarn, Thailand
We investigated complement in leprosy to detect its possible role in pathogenesis. Complement components, C3 proactivator (C3PA), CH50 and anticomplementary activity (AC) were determined in sera collected from lepromatous and tuberculoid leprosy. C3 was found increased in lepromatous leprosy and highly increased C3PA was found in both groups. Changes in other components lacked specific pattern. Increases in C3PA levels are believed to be due to aggregation of the increased serum immunoglobulins. C3 levels and CH50 levels in the present study agree with those in other reports. Development of AC occurred in lepromatous sera even during 2 days of storage at –80° C. AC found among freshly collected sera was probably due to aggregated immunoglobulins. The present study serves as a groundwork for future investigations.