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Abstract. Microscopic examination is the standard method for diagnosis of cutaneous and mucocutaneous leishmaniasis despite its low sensitivity. This study compared the diagnosis efficacy of microscopic examination versus polymerase chain reaction (PCR)-based methods and DNA sequencing using whole blood and skin lesion samples from patients with suspected leishmaniasis. The presence of Leishmania was determined by microscopy and amplification of 18S ribosomal RNA gene from blood and skin samples of 22 patients. Twenty individuals were positive for leishmaniasis. Microscopic analysis identified 85%, whereas PCR identified 100% of positive cases from skin and 90% from blood. Cytochrome b gene (cyt-b) amplification and sequencing identified Leishmania guyanensis, Leishmania shawi, and Leishmania naiffi from skin and blood samples. This study demonstrated the usefulness of whole blood and molecular techniques for the diagnosis and species identification of leishmaniasis.Leishmaniasis is a vector-borne disease caused by protozoan parasites of the Leishmania genus.

Leptin hormone controls food intake and has important immune functions. People with obesity show hypothalamic OBR resistance leading to high serum leptin levels. The increased risk to infections in people with obesity could be related to OBR resistance on immune cells. Few studies have compared the immune response between people with obesity matched with normal controls. This study compared the expression and response of the OBR on peripheral blood mononuclear cells (PBMCs) isolated from people with obesity and healthy controls. Fifteen subjects with obesity and age and sex matched normal weight controls participated in the study. Peripheral blood mononuclear cells were isolated from control and people with obesity after overnight fasting and were cultured with or without leptin or LPS for 24 hours. At the end of the treatment period, IL‐1β, IL‐6, and TNF‐α were measured by ELISA from culture supernatants. Also the expression of OBR on the surface of freshly isolated PBMCs was measured by flow cytometry. Data indicate that there was lower expression of OBR on PBMCs from subjects with obesity than from normal controls. Down‐regulation on the expression of OBR could indicate resistance to leptin stimulation. Also, there was lower production of IL‐1β, IL‐6, and TNF‐α in the supernatants of cultured PBMCs from subjects with obesity after leptin and LPS treatment than from normal controls. A lower cytokine production after leptin stimulation could also indicate OBR resistance due to lower expression and faulty activity of the receptor. Together these data are consistent with partial resistance of OBR on PBMCs from patients with obesity.

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