Models of Relapse of Experimental Visceral Leishmaniasis

• Published in: The Journal of infectious diseases 1996-04, Vol.173 (4), p.1041-1043
• Main Authors: Murray, Henry W., Hariprashad, June, Fichtl, Richard E.
• Format: Article
• Language: English
• Subjects: Animals; Antibodies; Biological and medical sciences; Chronic Disease; Concise Communications; Disease Models, Animal; Human protozoal diseases; Immunologic Deficiency Syndromes - parasitology; Infections; Infectious diseases; Leishmania donovani; Leishmania donovani - pathogenicity; Leishmaniasis, Visceral - immunology; Leshmaniasis; Liver; Lymphocyte Depletion; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Nude; Necrosis; Parasite hosts; Parasites; Parasitic diseases; Protozoal diseases; Relapse; T lymphocytes; T-Lymphocytes - immunology; Time Factors; Tropical medicine; Visceral leishmaniasis
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1093/infdis/173.4.1041

To establish models for studying recurrence of visceral leishmaniasis, a growing problem in T cell-deficient patients, two approaches were investigated: treatment of euthymic BALB/c mice with quiescent Leishmania donovani infection with T cell-depleting or anti-cytokine antibodies and serial observation of acutely infected nude BALB/c mice after an initial antileishmanial response induced by amphotericin B treatment. In chronically infected euthymic mice, maintenance of acquired immunity and prevention of relapse required CD4 cells and a multicytokine-dependent mechanism involving endogenous interleukin-2, interferon-γ, and tumor necrosis factor-α. Acutely infected nude mice responded to amphotericin B with a ⩾85% reduction in liver parasite burdens; however, after a brief lag, visceral infection readily recurred in the posttreatment period. Both models may be useful for testing experimental interventions designed to reduce relapse of previously controlled visceral leishmaniasis in T cell-deficient hosts.