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
A panel of eight Trypanosoma cruzi antigens produced by recombinant DNA techniques was used to compare the reactivity of IgG specificities in the sera from 45 chronic Chagas' disease patients with different clinical symptoms (cardiac disease, gastro-intestinal lesions, and combined syndrome) with those present in the sera from 55 asymptomatic patients in Chile. All of the serum samples were first characterized for antibody to T. cruzi epimastigotes by immunofluorescence assay. All of the Chagas' disease sera were reactive, but none of five healthy controls whose sera were also tested had antibodies against the fixed parasites. A dot-blot assay was then performed to evaluate the serum reactivity against recombinant DNA clones 1, 2, 13, 26, 30, 36, 54, and SAPA (shed acute phase antigen). These recombinant antigens were recognized by a large proportion of the sera collected from the Chilean patients. Ninety-five percent of the serum samples reacted with one or more of the recombinant clones. Analysis of the reactivity with individual fusion proteins showed that 88% of these sera reacted with clones 1 and 2, and 78% reacted with clone 13. Differences in reactivity to clones number 13, 30, and SAPA were observed when symptomatic and asymptomatic patients were compared. These differences in reactivity were statistically significant (P < 0.01) according to Fisher's exact test.