Amastigotes from L. (L.)amazonensis (La), L. (L.)venezuelensis (Lv), L. (V.)brasiliensis (Lb), and L. (L.)chagasi (Lch) were cultured in a free cells liquid culture medium. Patients ( ) from a cutaneous leishmaniasis (CL) hyperendemic region receiving different treatments were followed up from January 1994 to August 2000. Time for remission of lesions were spontaneous remission (SR) 7 weeks; Glucantime (Glu) chemotherapy 9 weeks; immunotherapy with La, Lv, Lb, and Lch amastigotes Tosyl-Lysil Chloromethyl-ketone (TLCK) treated and Nonidet P-40(NP-40) extracted (VT) 7 weeks. Delayed type hypersensitivity (DTH) response with leishmanine intradermic reaction (IDR) was higher in CL patients than healthy controls ( ) and increased in active secondary versus primary infection ( ) with diagnostic value 1.74 for active infection and 1.81 postclinical remission. Antibodies to amastigotes characterized by Enzyme Linked Immunosorbent Assay (ELISA) decreased in sera postclinical remission versus active infections ( ), with a diagnostic value from 1.50 to 1.84. Immunoblottings antigenic bands frequency as well as Integral Optical Density (IOD) Area Densitometry decreased with sera from SR, after Glu or VT treatments in CL volunteers. Intracellular parasitism is due to normal antibodies recognizing parasite antigens after inoculation by vector. VT vaccine induced mainly cellular immunity, for remission of lesions and protection from CL infection. 1. Introduction Leishmaniasis is a global zoonosis from the tropics and subtropics, with humans serving as accidental hosts. Due to disease prevalence, one-tenth of the world’s populations (700 million people) are at risk of infection. Globally, there are 12 million cases, and the incidences of visceral (VL) and CL infections are approximately 0.5 and 1–1.5 million new cases each year, respectively [1, 2]. In a sample population ( ), parasites were obtained from 85 patients (52.5%), and were isolated from the blood by cultures of 50 patients (30.9%). Isoenzyme analysis confirmed that the organisms in blood and skin were the same, which underlines the invasive potential of the parasite that escaped the skin [3]. Extracellular procyclic promastigotes in the vector mature to metacyclic promastigotes (motile), that evolve to amastigotes (nonmotile) once they enter cells in the vertebrate host after the insect bite. The amastigote eventually evolves back to the promastigote form in the vector after a blood meal in infected hosts, closing the cycle. The mature infective metacyclic promastigotes have surface glycosyl inositol
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