Molecular Characterization of the cry Gene profile of Bacillus thuringiensis Isolated from a Caribbean Region of Colombia.

In order to characterize native strains of Bacillus thuringiensis of the Colombian Caribbean with toxic effect against insect vectors, 28 samples of bacteria identified as B. thuringiensis were isolated from different soils and muds around the city of Valledupar. Using a biological test, five isolates of B.

Detection of high percentage of Trypanosoma cruzi infection, the etiologic agent of Chagas disease, in wild populations of Colombian Caribbean triatomines.

In Colombia it is estimated that about 900,000 persons are infected with T. cruzi. There are 25 triatomine species and 5 of them have been reported infected with T.

Trypanosoma cruzi Calreticulin Topographical Variations in Parasites Infecting Murine Macrophages.

Trypanosoma cruzi calreticulin (TcCRT), a 47-kDa chaperone, translocates from the endoplasmic reticulum to the area of flagellum emergence. There, it binds to complement components C1 and mannan-binding lectin (MBL), thus acting as a main virulence factor, and inhibits the classical and lectin pathways. The localization and functions of TcCRT, once the parasite is inside the host cell, are unknown.

[Estimation of costs caused by cystic echinococcosis].

Background: Hydatid disease or cystic echinococcosis, caused by the parasite Echinococcus granulosus, has a worldwide distribution, affecting people of working age and can cause high levels of morbidity and even death.

Aim: To estimate the economic impact at the human and animal level caused by the disease in Chile.

Material And Methods: We analyzed information about the disease obtained from reports and publications emanated from the Chilean Ministry of Health, United Nations Food and Agriculture Organization, the U.

Detection of the G3 genotype of Echinococcus granulosus from hydatid cysts of Chilean cattle using COX1 and ND1 mitochondrial markers.

For a deeper understanding of the phylogenetic relationships of Echinococcus genotypes and species in different intermediate hosts, we analyzed samples from human and bovine hydatid cysts. For this, segments of the cytochrome oxidase (COX1) and NADH dehydrogenase (ND1) mitochondrial genes were used. To obtain sufficient amounts of the ND1 marker to be sequenced properly, a new variant of the PCR assay was implemented.

Microsatellite loci-based distribution of Trypanosoma cruzi genotypes from Chilean chronic Chagas disease patients and Triatoma infestans is concordant with a specific host-parasite association hypothesis.

The objective of this study was to investigate if there is specific host-parasite association in Chilean populations of Trypanosoma cruzi. For this purpose, two groups of parasites were analyzed, one from chronic chagasic patients, and the other from Triatoma infestans triatomines in three regions of the country. The first group consisted of four types of samples: parasites from peripheral blood of non-cardiopathic T.

Microsatellite marker analysis shows differentiation among Trypanosoma cruzi populations of peripheral blood and dejections of Triatoma infestans fed on the same chronic chagasic patients : microsatellite marker analysis and T. cruzi.

To investigate whether Trypanosoma cruzi populations found in chagasic cardiopathic and non-cardiopathic patients are genetically differentiated, three molecular microsatellite markers were analysed. This analysis was also applied to compare T. cruzi samples from peripheral blood or dejections of Triatoma infestans fed on the blood of the same patients.

Trypanosoma cruzi calreticulin: a novel virulence factor that binds complement C1 on the parasite surface and promotes infectivity.

In Trypanosoma cruzi, calreticulin (TcCRT) translocates from the endoplasmic reticulum (ER) to the area of flagellum emergence. We propose herein that the parasite uses this molecule to capture complement C1, in an infective apoptotic mimicry strategy. Thus, TcCRT/C1 interactions, besides inhibiting the classical pathway of complement activation as previously shown in our laboratories, will also promote infectivity.

Molecular mechanisms involved in the inactivation of the first component of human complement by Trypanosoma cruzi calreticulin.

Trypanosoma cruzi (T. cruzi), the agent of Chagas' disease, the sixth most important neglected tropical disease worldwide, causes 50,000 deaths per year in Latin America. T.

Phylogenetic analysis of microsatellite markers further supports the two hybridization events hypothesis as the origin of the Trypanosoma cruzi lineages.

To better understand the evolution of the etiologic agent of Chagas disease, we cloned and sequenced 25 alleles from five Tripanosoma cruzi microsatellite markers. The study of the sequences showed highly conserved alleles present in T. cruzi clones belonging to TCI, TCIIc, and TCIIe.

Differential distribution of Trypanosoma cruzi clones in human chronic chagasic cardiopathic and non-cardiopathic individuals.

PCR and Southern blot hybridization were used to determine the distribution of Trypanosoma cruzi clones in 37 chronic chagasic cardiopathic and non-cardiopathic patients. Parasite DNA amplified from peripheral blood or dejections of Triatoma infestans fed on patient blood was hybridized with probes containing hypervariable minicircle nucleotide sequences capable of detecting three sublineages of T. cruzi.

Comparison of Trypanosoma cruzi detection by PCR in blood and dejections of Triatoma infestans fed on patients with chronic Chagas disease.

In this study, we compare the sensitivity of detecting Trypanosoma cruzi in dejections of Triatoma infestans nymphs that had fed on the blood of chronic chagasic patients, with detection of T. cruzi in peripheral blood, using a polymerase chain reaction assay (PCR-D and PCR-B, respectively). Fifty-seven chronic patients were evaluated who were positive (group I) or negative (group II) by xenodiagnosis (XD).

Variation in Trypanosoma cruzi clonal composition detected in blood patients and xenodiagnosis triatomines: implications in the molecular epidemiology of Chile.

To identify Trypanosoma cruzi clones from chronically infected individuals, they were transferred to triatomines by the xenodiagnosis test (XD) with Triatoma infestans. Polymerase chain reaction (PCR) and hybridization assays were performed to detect minicircle DNA in human blood samples and triatomine feces, using probes to determine the T. cruzi clones present.

Dissimilar distribution of Trypanosoma cruzi clones in humans after chemotherapy with allopurinol and itraconazole.

Objectives: The aim of this work was to study the distribution of Trypanosoma cruzi clones after treatment failure with itraconazole or allopurinol in infected humans.

Methods: Blood samples from treated and untreated individuals were used to detect T. cruzi by PCR assays and were confirmed by hybridization tests using total kinetoplast DNA as a universal probe.

[No association between persistence of the parasite and electrocardiographic evolution in treated patients with Chagas disease].

Background: At the present time the assessment of results of treatment of Chagas disease is mainly parasitological. Anti Trypanosoma cruzi IgGs remain positive practically lifelong and electrocardiographic tracings are not usually used as criteria of improvement.

Aim: To determine, in a long term follow up, if electrocardiographic evolution is associated with the persistence of the parasite in treated patients with chronic Chagas disease.

Use of polymerase chain reaction (PCR) and hybridization assays to detect Trypanosoma cruzi in chronic chagasic patients treated with itraconazole or allopurinol.

The presence of Trypanosoma cruzi in chronic chagasic patients with negative xenodiagnosis (XD) after 6 years following completion of therapy with either itraconazole or allopurinol was assessed by polymerase chain reaction (PCR) and hybridization assays. A 330-bp DNA fragment amplified from the hypervariable regions of T. cruzi kinetoplastid minicircles was hybridized with total 32P-labeled kinetoplast DNA as probes.

The classical activation pathway of the human complement system is specifically inhibited by calreticulin from Trypanosoma cruzi.

The high resistance of Trypanosoma cruzi trypomastigotes, the causal agent of Chagas' disease, to complement involves several parasite strategies. In these in vitro studies, we show that T. cruzi calreticulin (TcCRT) and two subfragments thereof (TcCRT S and TcCRT R domains) bind specifically to recognition subcomponents of the classical and lectin activation pathways (i.

Cytotoxicity and trypanocidal activity of nifurtimox encapsulated in ethylcyanoacrylate nanoparticles.

The aim of the present study was to study the trypanocidal activity of nanoparticles loaded with nifurtimox in comparison with the free drug against Trypanosoma cruzi, responsible for Chagas' disease. Ethylcyanoacrylate nanoparticles acted as the delivery system into cells. As the obligate replicative intracellular form is amastigote, in vitro studies were performed on this form of parasite as well as on cell culture derived trypomastigotes.

[Immunophenotyping of peripheral blood lymphocytes from Chilean chronic chagasic patients by flow cytometry].

Background: Cellular immune mechanisms of the resistance to infection by T cruzi as well as the pathogenesis of Chagas disease are still controversial.

Aim: To quantify and analyse the peripheral blood immune cells from chagasic and non chagasic patients by flow cytometry.

Patients And Methods: Peripheral blood samples were taken from 21 individuals seropositive for Chagas disease, under no specific treatment.