Mangoud A M, Ramadan M E, Morsy T A, Amin A M, Mostafa S M
Early Cancer Detection Unit, Faculty of Medicine, Zagazig University, Egypt.
J Egypt Soc Parasitol. 1997 Dec;27(3):689-702.
In the 1980s, infantile visceral leishmaniasis was documented in Al Agamy (Alexandria). The causative agent is Leishmania d. infantum and the insect vector is Phlebotomus langeroni. In this paper, Syrian golden hamsters were chosen as a model animal for histopathological studies of L. d. infantum. Twenty four male hamsters were experimentally infected with L.d. infantum. Every week, two hamsters were sacrificed and parts from the liver, heart, lung, spleen, small intestine and kidney were paraffin sectioned and stained with haematoxylin and eosin or with Giemsa stain. The leishmanial granuloma was the main histopathological changes and the liver was the main organ affected. Leishmanial granulomas were common in the liver, but few in lung and small intestine. The hepatic granulomas increased in surface areas and in number in the late stage of the infection (< 6 weeks). They were formed mainly of histiocytes, less lymphocytes and very few eosinophils with necrosis inside and bridging in between granulomas mainly occurred in the late stage of infection. Neither fibrosis nor peripheral delimitation was seen. Kupffer cell hyperplasia was seen throughout the experimental period (12 weeks). The spleen showed expansion of the red pulp and atrophy of the white pulp. The kidney showed mesangial cell proliferation and the mesangial matrix increased accompanied with amyloid deposition. All the tissue sections were photographed and the results were discussed.
