Many aspects of the human asymptomatic visceral leishmaniasis (VL) remain not elucidated, and moreover, almost all the data come from highly endemic areas. The recent appearance of American VL (AVL) in the northeastern region of the state of São Paulo, Brazil, offered a good opportunity for further understanding. We present the preliminary results from a seroprevalence study on AVL in humans in Araçatuba, São Paulo. This was a cross-sectional survey on a random sample of the population (one-stage simple random sampling) in two areas, using rK39 dipstick tests. The sex ratios and age distributions in the two areas were comparable. Detectable antibodies were found in 23 subjects (20%) in area A1 and in 6 subjects (4.8%) in area A2. There was no significant difference in age distribution of seropositivity between the areas. We observed a difference in asymptomatic infection rates between the two areas, possibly associated with socioeconomic levels and transmission intensity.

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Leishmaniasis is a parasitic disease that leads to chronic inflammation. Macrophages, depending on their activation state, are either hosts or killers of the parasites. Downregulation of nitric oxide (NO) synthesis by the parasite infecting the macrophages has been proposed to be an important evading mechanism based on in vitro studies. We confirmed inhibition of NO release by macrophages infected with Leishmania amazonensis in vitro. To examine the role of the parasite in regulating NO production in vivo, we monitored systemic NO levels elicited by challenging naive and L. amazonensis-infected BALB/c mice with lipopolysaccharide (LPS). Animals were challenged after 1, 2, 6, and 9 wk of infection. NO production was monitored by electron paramagnetic resonance spectroscopy as the levels of hemoglobin nitrosyl complexes (HbNO) present in the animal's blood. No significant differences in HbNO levels were observed between LPS-treated naive and inoculated mice at any time during infection. To control for increased macrophage numbers in infected mice, naive mice were injected with a macrophage cell line before LPS challenge; this treatment did not increase produced NO levels. The results argue against a major role for the parasite in downregulating NO production in vivo.

Leishmaniasis is a parasitic disease that leads to chronic inflammation. Macrophages, depending on their activation state, are either hosts or killers of the parasites. Downregulation of nitric oxide (NO) synthesis by the parasite infecting the macrophages has been proposed to be an important evading mechanism based on in vitro studies. We confirmed inhibition of NO release by macrophages infected with Leishmania amazonensis in vitro. To examine the role of the parasite in regulating NO production in vivo, we monitored systemic NO levels elicited by challenging naive and L. amazonensis-infected BALB/c mice with lipopolysaccharide (LPS). Animals were challenged after 1, 2, 6, and 9 wk of infection. NO production was monitored by electron paramagnetic resonance spectroscopy as the levels of hemoglobin nitrosyl complexes (HbNO) present in the animal's blood. No significant differences in HbNO levels were observed between LPS-treated naive and inoculated mice at any time during infection. To control for increased macrophage numbers in infected mice, naive mice were injected with a macrophage cell line before LPS challenge; this treatment did not increase produced NO levels. The results argue against a major role for the parasite in downregulating NO production in vivo.

Background and Methods: In this study, we investigated the effect of 8-bromoguanosine (8Brguo), an immunostimulatory compound, in a murine model of experimental cutaneous leishmaniasis. Results: The results indicated that treatment by intraperitoneal administration of 8Brguo (150 mg/kg once daily for 1 week and thereafter once weekly for 1 month) diluted in Tween-80 produces an effect similar to that of treatment with the classical antimonial drug, Glucantime, in Leishmania amazonensis-infected CBA/J mice. While complete cure did not occur, animals treated with the nucleoside had small lesions in the infected footpad and delayed surface ulceration. Studies involving examination of serum glutamic pyruvic transaminase activity, concentration of urea, blood pathology and histology of the spleen, kidney and liver showed no apparent toxicity of the nucleoside in treated mice. Conclusion: The protective in vivo effect during murine leishmaniasis as well as the lack of apparent toxicity of 8Brguo as attested by blood/serum pathology and histology from treated mice encourage further studies of C8-substituted guanine ribonucleosides, such as 8Brguo, as new leishmanial drugs and as modifiers of the immunological response to combat infections with intracellular pathogens.