Late Metastatic Leishmaniasis in the Mouse

A Model for Mucocutaneous Disease

A. Barral Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Medicine, University of Arizona, Bethesda, Maryland 20205

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E. A. Petersen Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Medicine, University of Arizona, Bethesda, Maryland 20205

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D. L. Sacks Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Medicine, University of Arizona, Bethesda, Maryland 20205

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F. A. Neva Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Medicine, University of Arizona, Bethesda, Maryland 20205

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BALB/c, C57Bl/6 and (BALB/c × C57Bl/6)F1 mice all proved susceptible to infection by a strain of Leishmania isolated from a Central Brazilian with espundia. The course of disease differed markedly between BALB/c and C57Bl/6 mice. BALB/c mice suffered from a rapidly progressive and widely metastatic, but non-ulcerative, disease resembling diffuse cutaneous leishmaniasis. In contrast, C57Bl/6 mice initially contained parasite multiplication effectively and appeared clinically cured. However, the parasite could persistently be cultured up to about 1 year post-infection. At that time, the parasite load in the infected footpad increased and a patent disease developed characterized by distinctive ulcerative metastases with destruction of soft-tissue in the nasal region similar to the one observed in espundia. Development of disease in both strains of mice was associated with depression of cell-mediated immunity as monitored by delayed-type hypersensitivity in vivo and lymphocyte transformation in vitro. Thus, our study suggests that diffuse cutaneous leishmaniasis and espundia can be caused by the same strain of parasite, and that the particular clinical expression in the individual mouse is determined by the host response.

Author Notes

Present address: Centro de Pesquizas gonçalo Mohiz, Rua Valdemar Falcão, 121-Brotas, 40.000 Salvador-Bahia, Brazil.

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