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
Servico de Imunologia do Hospital Universitario Prof. Edgard Santos, Faculdade de Medicina da Universidade Federal da Bahia, Nucleo de Medicina Tropical e Nutricao da Universidade de Brasilia, Salvador, Bahia, Brazil
In patients with cutaneous leishmaniasis in areas of Leishmania braziliensis transmission, ulcers may heal without therapy. In the present study, we evaluated the T cell responses of 10 subjects who two years earlier had a rapidly (less than three months) self-healing cutaneous disease. The immunologic responses of these cases were determined by intradermal skin test, measurements of antibodies, lymphocyte proliferative responses, and interferon-γ (IFN-γ) production in cultures stimulated with Leishmania antigens. These data were compared with those observed in 10 other patients with active cutaneous and mucosal leishmaniasis. Evidence of strong lymphocyte blastogenesis and IFN-γ production was observed in eight of 10 patients with self-healing cutaneous leishmaniasis, with stimulation indices ranging from 32 to 506, and IFN-γ levels ranging from 500 to 2,900 pg/ml. The mean ± SD stimulation index of the lymphocyte proliferative responses (288 ± 247) and the mean ± SD of IFN-γ production after stimulation with Leishmania antigen (970 ± 960 pg/ml) in subjects with self-healing cutaneous leishmaniasis were similar (P > 0.05) to those observed in patients with mucosal disease (stimulation index = 308 ± 282 and IFN-γ level = 838 ± 819 pg/ml). These responses were higher (P < 0.01) than those observed in patients with active cutaneous leishmaniasis (stimulation index = 50 ± 82 and IFN-γ level = 264 ± 336 pg/ml). The mean ± SD induration of skin test reactions in subjects with self-healing cutaneous leishmaniasis (23 ± 14 mm) and in patients with mucosal disease (18 ± 6 mm) were greater (P < 0.01) than those observed in patients with active cutaneous leishmaniasis (10 ± 6 mm). In contrast with these parameters of T cell response, the mean ± SD absorbances of the enzyme-linked immunosorbent assay to detect antibodies against Leishmania in patients with self-healing cutaneous leishmaniasis (0.017 ± 0.008) was lower (P < 0.05) than those observed in patients with active cutaneous leishmaniasis (0.067 ± 0.014) or in patients with mucosal leishmaniasis (0.104 ± 0.056). These data indicate that subjects with self-healing cutaneous leishmaniasis have a strong T cell response to leishmania antigens. This response may have been involved in control of their Leishmania infection.