Prepared under the auspices of The American Society of Clinical Pathologists. By John A. Kolmer, M.D., Dr.P.H., D.Sc., LL.D., and Fred Boerner, V.M.D. Assisted by C. Z. Garber, A.B., M.D., and Committees of The American Society of Clinical Pathologists. Pp. I–XXII. 1–663. D. Appleton and Company, New York and London, 1931
Institute of Tropical Medicine, Center for Medical Parasitology, Institute for Medical Microbiology and Immunology, University of Copenhagen, Department of Infectious Diseases and Department of Clinical Microbiology, National University Hospital of Denmark (Rigshospitalet), Department of Medicine and Institute of Endemic Diseases, University of Khartoum, Faculty of Medicine, Wadi El Niel University, Khartoum, Sudan
The pathology of cutaneous leishmaniasis in Sudan, where the disease is caused by Leishmania major, was studied by light and electron microscopy. Lesions were classified into four distinct groups based on the ratio of different cell types, especially lymphocytes, macrophages, and plasma cells in the inflammatory infiltrate, and the formation of compact epithelioid granulomas or the presence of necrosis. In the lesions, there was a positive correlation between the number of lymphocytes and the number of activated macrophages and epithelioid cells. We suggest that the parasites are eliminated from the lesion by two processes: 1) a lytic mechanism in which parasites are lysed within activated macrophages and 2) necrosis of parasitized macrophages. Morphologic evidence for these two mechanisms of parasite elimination was detected by both light and electron microscopy. The evolution of the pathology of the lesions was followed by rebiopsy when the lesion had regressed in size under antileishmanial therapy.