Visceral spreading depletion of thymus-dependent regions and amyloidosis in mice and hamsters infected intradermally with Leishmania isolated from Sudanese cutaneous leishmaniasis.

Eighteen outbred mice and 21 golden hamsters were each inoculated intradermally with 2 X 10(6) Leishmania amastigotes obtained from 1 case of Sudanese cutaneous leishmaniasis. The skin lesions, spleen, lymph nodes, liver and kidney were examined by light-, polarizing-, and electron microscope at 5, 9 and 18 weeks after inoculation. The aim of the investigations was to follow the development of the inflammatory reaction and the change of the morphology of the lymphoid organs during the infection. In all the mice and in the majority of the hamsters visceral leishmaniasis developed which was characterized by a "noncure" type of cellular reaction, a selective T-cell depletion in the lymph nodes and the spleen, and the development of a reactive, systemic amyloidosis. These findings point to the failure of the acquired resistance against Leishmania to develop. In some of the hamsters the response was of the "cure" type without the development of amyloidosis. At the site of the inoculation the lesions healed suggesting the positive role of necrosis and the elimination of the parasites through the ulcer in the healing process. Electron microscopy showed erythrophagocytosis in the spleen of the 2 mice examined presenting an experimental evidence of the destruction of the red blood cells, which is a common feature of human kala-azar.