Lack of a nitric-oxide response during the course of Leishmania infantum infection in the golden hamster (Mesocricetus auratus), with or without treatment with liposomal amphotericin B.

Liver and spleen volumes and serum concentrations of nitrate (the end-product of NO in vivo), albumin, gamma-globulin, protein, creatine and urea were measured during the course of progressive infections with Leishmania infantum MON-1 (MHOM/PR/93/CRE29) in 10 Syrian golden hamsters. Each hamster was infected by intraperitoneal injection with 4 x 10(7) promastigotes. Five of the infected animals were treated, with 6 mg liposomal amphotericin B (L-AmB)/kg given by intracardiac injection, on day 107 post-infection (p.i.). Compared with those in the uninfected hamsters used as controls, the liver volumes in the infected animals became significantly enlarged by day 40 p.i. (38% larger than the controls; P < 0.001) whereas significant enlargement of the spleen was first detected on day 72. Each infected animal had detectable serum levels of antileishmanial antibodies on day 72. There were significant elevations in gamma-globulin concentration as early as day 40 (P < 0.05) but significant falls in albumin concentrations were only detected from day 107 (P < 0.001). Nitrate, creatinine and urea concentrations remained unchanged during the course of infection, even after L-AmB treatment. Serum nitrate levels were not enhanced by L. infantum infection nor by the L-AmB treatment which induced a 98.2% decrease in parasite burden. The lack of NO production in visceral leishmaniasis, with or without L-AmB treatment, points to the unresponsiveness of inducible nitric oxide synthase in this rodent model.