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Sent on Wednesday, 2011 Jun 01Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Parasitol Res. 2011 May 31. [Epub ahead of print]Seroepidemiology of Toxoplasma gondii, Neospora caninum, and Leishmania spp. infections and risk factors for cats from Brazil.Coelho WM, do Amarante AF, Apolinário JD, Coelho NM, de Lima VM, Perri SH, Bresciani KD.SourceUniversidade Estadual Paulista-UNESP, Campus de Araçatuba-SP, Rua Clóvis Pestana, 793, Araçatuba, 16050-680, São Paulo, Brazil, willianmarinho@hotmail.com. AbstractThe seroprevalence of infection by Toxoplasma gondii, Neospora caninum, and Leishmania spp. was detected through an indirect immunofluorescence in 70 cats from the Andradina Municipality, São Paulo State, Brazil. Anti-T. gondii antibodies (titer >64) were detected in 15.7% (11/70) of animals, whereas positivity for N. caninum (titer 16) was not observed in any animal. Of the cats from urban and rural areas, 10.4% (5/48) and 27.2% (6/22) were positive for T. gondii, respectively. Breed, age, food, and contact with animals of other species were significant for considering the positivity for T. gondii (P ≤ 0.0001). Cats having access to streets (17.1%, 11/64), cats cohabiting with rats (19.6%, 10/51), and cats feeding on homemade food and raw milk (27.2%, 6/22) were positive for T. gondii. In addition, 4.2% (3/70) of the cats were positive for Leishmania spp. by ELISA technique and negative by IFAT without coinfection with T. gondii and Leishmania spp. There was no serological positivity against feline immunodeficiency virus or feline leukemia virus. In conclusion, T. gondii infection in part of the feline population from Andradina is not linked to immunosuppressions or coinfections but probably to postnatal infection in association with the type of diet and presence of rats. |
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| 2. | Comp Biochem Physiol B Biochem Mol Biol. 2011 May 23. [Epub ahead of print]Arginine kinase in Phytomonas, a trypanosomatid parasite of plants.Canepa GE, Carrillo C, Miranda MR, Sayé M, Pereira CA.SourceLaboratorio de Biología Molecular de Trypanosoma cruzi (LBMTC), Instituto de Investigaciones Médicas Alfredo Lanari, Universidad de Buenos Aires and CONICET, Buenos Aires, Argentina. AbstractPhytomonas are trypanosomatid plant parasites closely related to parasites that cause several human diseases. Little is known about the biology of these organisms including aspects of their metabolism. Arginine kinase (E.C. 2.7.3.3) is a phosphotransferase which catalyzes the interconversion between the phosphagen phosphoarginine and ATP. This enzyme is present in some invertebrates and is a homolog of another widely distributed phosphosphagen kinase, creatine kinase. In this work, a single canonical arginine kinase isoform was detected in Phytomonas Jma by enzymatic activity assays, PCR, and Western Blot. This arginine kinase is very similar to the canonical isoforms found in T. cruzi and T. brucei, presenting about 70% of amino acid sequence identity and a very similar molecular weight (40kDa). The Phytomonas phosphagen system seems to be very similar to T. cruzi, which has only one isoform, or T. brucei (three isoforms); establishing a difference with other trypanosomatids, such as Leishmania, which completely lacks phosphagen kinases, probably by the presence of the arginine-consuming enzyme, arginase. Finally, phylogenetic analysis suggests that Kinetoplastids' arginine kinase was acquired, during evolution, from the arthropod vectors by horizontal gene transfer. Copyright © 2011. Published by Elsevier Inc. |
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| 3. | Fitoterapia. 2011 May 23. [Epub ahead of print]Antitrypanosomal sesquiterpene lactones from Saussurea costus.Ju lianti T, Hata Y, Zimmermann S, Kaiser M, Hamburger M, Adams M.SourceDivision of Pharmaceutical Biology, University of Basel, CH-4056 Basel, Switzerland; Faculty of Pharmacy, Pancasila University, 12640 Jakarta, Indonesia. AbstractIn the course of a larger screen of 1800 plant and fungal extracts, the ethyl acetate extract of Saussurea costus roots potently inhibited the growth of Trypanosoma brucei rhodesiense. Subsequent HPLC based activity profiling led to the identification of the sesquiterpene lactones arbusculin B (1), α-cyclocostunolide (2), costunolide (3), and dehydrocostuslactone (4). They were tested for in vitro antitrypanosomal activities and cytotoxicity alongside the structurally related sesquiterpene lactones parthenolide (5), zaluzanin D (6), and eupatoriopicrin (7), and had IC(50)s between 0.8 and 22μM. Cytotoxic IC(50)s were from 1.6 to 19μM, and selectivity indices from 0.5 to 6.5. Copyright © 2011. Published by Elsevier B.V. |
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| 4. | Cell Microbiol. 2011 May 30. doi: 10.1111/j.1462-5822.2011.01602.x. [Epub ahead of print]Promastigote to amastigote differentiation of Leishmania is markedly delayed in the absence of PERK eIF2alpha kinase-dependent eIF2alpha phosphorylation.Chow C, Cloutier S, Dumas C, Chou MN, Papadopoulou B.SourceGenera Biosystems, Small Technologies Cluster, 1 Dalmore Drive, Scoresby, Victoria 3179, Australia Infectious Disease Research Center, CHUL Research Center and Department of Microbiology and Immunology, Faculty of Medicine, Laval University, Quebec, Canada Impres Pharma, Waterloo, Ontario, Canada. AbstractThe parasitic protozoan Leishmania is the etiological agent of human leishmaniasis worldwide. It undergoes cellular differentiation from the sandfly promastigote form into amastigotes within mammalian macrophages, a process that is essential for its intracellular survival. Here, we characterized the Leishmania infantum PERK eIF2alpha kinase homologue and addressed its role in the parasite's cytodifferentiation. We show that Leishmania PERK is an endoplasmic reticulum (ER) transmembrane protein that largely colocalizes with the ER BiP chaperone. The Leishmania PERK catalytic kinase domain undergoes autohyperphosphorylation and phosphorylates the translation initiation factor 2-alpha subunit (eIF2alpha) in vitro at threonine 166. We also report that PERK is post-translationally regulated specifically in the intracellular stage of the parasite or under ER stress, most likely through extensive autohyperphosphorylation. We have generated a PERK dominant negative mutant overexpressing a truncated PERK protein lacking the N-terminal luminal domain and showed that this mutant is impaired in eIF2alpha phosphorylation in response to ER stress or during amastigote differentiation. Most importantly, we showed that lack of eIF2alpha phosphorylation markedly delays the Leishmania differentiation process towards amastigote forms both in parasites grown axenically or within macrophages. These data highlight the importance of PERK eIF2alpha kinase-dependent eIF2alpha phosphorylation in the intracellular development of Leishmania. © 2011 Blackwell Publishing Ltd. |
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| 5. | Trop Med Int Health. 2011 May 30. doi: 10.1111/j.1365-3156.2011.02803.x. [Epub ahead of print]Monitoring drug effectiveness in kala-azar in Bihar, India: cost and feasibility of periodic random surveys vs. a health service-based reporting system.Malaviya P, Singh RP, Singh SP, Hasker E, Ostyn B, Shankar R, Boelaert M, Sundar S.SourceDepartment of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India Epidemiology and Disease Control Unit, Department of Public Health, Institute of Tropical Medicine, Antwerp, Belgium. AbstractObjective: In 2009, a random survey was conducted in Muzaffarpur district to document the clinical outcomes of visceral leishmaniasis patients (VL) treated by the public health care system in 2008, to assess the effectiveness of miltefosine against VL. We analysed the operational feasibility and cost of such periodic random surveys as compared with health facility-based routine monitoring. Methods: A random sample of 150 patients was drawn from registers kept at Primary Health Care centres. Patient records were examined, and the patients were located at their residence. Patients and physicians were interviewed with the help of two specifically designed questionnaires by a team of one supervisor, one physician and one field worker. Costs incurred during this survey were properly documented, and vehicle log books maintained for analysis. Results: Hundred and 39 (76.7%) of the patients could be located. Eleven patients were not traceable. Per patient, follow-up cost was US$ 15.51 and on average 2.27 patients could be visited per team-day. Human resource involvement constituted 75% of the total cost whereas involvement of physician costs 51% of the total cost. Conclusion: A random survey to document clinical outcomes is costly and labour intensive but gives probably the most accurate information on drug effectiveness. A health service-based retrospective cohort reporting system modelled on the monitoring system developed by tuberculosis programmes could be a better alternative. Involvement of community health workers in such monitoring would offer the additional advantage of treatment supervision and support. © 2011 Blackwell Publishing Ltd. |
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| 6. | PLoS Negl Trop Dis. 2011 Feb 1;5(2):e953.Trypanosoma cruzi utilizes the host low density lipoprotein receptor in invasion.Nagajyothi F, Weiss LM, Silver DL, Desruisseaux MS, Scherer PE, Herz J, Tanowitz HB.SourceDepartment of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA. fnu.nagajyothi@einstein.yu.edu AbstractBACKGROUND:Trypanosoma cruzi, an intracellular protozoan parasite that infects humans and other mammalian hosts, is the etiologic agent in Chagas disease. This parasite can invade a wide variety of mammalian cells. The mechanism(s) by which T. cruzi invades its host cell is not completely understood. The activation of many signaling receptors during invasion has been reported; however, the exact mechanism by which parasites cross the host cell membrane barrier and trigger fusion of the parasitophorous vacuole with lysosomes is not understood. METHODOLOGY/PRINCIPAL FINDINGS:In order to explore the role of the Low Density Lipoprotein receptor (LDLr) in T. cruzi invasion, we evaluated LDLr parasite interactions using immunoblot and immunofluorescence (IFA) techniques. These experiments demonstrated that T. cruzi infection increases LDLr levels in infected host cells, inhibition or disruption of LDLr reduces parasite load in infected cells, T. cruzi directly binds recombinant LDLr, and LDLr-dependent T. cruzi invasion requires PIP2/3. qPCR analysis demonstrated a massive increase in LDLr mRNA (8000 fold) in the heart of T. cruzi infected mice, which is observed as early as 15 days after infection. IFA shows a co-localization of both LDL and LDLr with parasites in infected heart. CONCLUSIONS/SIGNIFICANCE:These data highlight, for the first time, that LDLr is involved in host cell invasion by this parasite and the subsequent fusion of the parasitophorous vacuole with the host cell lysosomal compartment. The model suggested by this study unifies previous models of host cell invasion for this pathogenic protozoon. Overall, these data indicate that T. cruzi targets LDLr and its family members during invasion. Binding to LDL likely facilitates parasite entry into host cells. The observations in this report suggest that therapeutic strategies based on the interaction of T. cruzi and the LDLr pathway should be pursued as possible targets to modify the pathogenesis of disease following infection. |
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| 7. | PLoS Negl Trop Dis. 2011 Feb 22;5(2):e1008.Sleeping sickness elimination in sight: time to celebrate and reflect, but not relax.Aksoy S.SourceYale School of Public Health, New Haven, Connecticut, USA. Serap.Aksoy@yale.edu |
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| 8. | PLoS Negl Trop Dis. 2011 Feb 22;5(2):e970.A history of chagas disease transmission, control, and re-emergence in peri-rural La Joya, Peru.Delgado S, Castillo Neyra R, Quispe Machaca VR, Ancca Juárez J, Chou Chu L, Verastegui MR, Moscoso Apaza GM, Bocángel CD, Tustin AW, Sterling CR, Comrie AC, Náquira C, Cornejo del Carpio JG, Gilman RH, Bern C, Levy MZ.SourceSchool of Geography and Development, University of Arizona, Tucson, Arizona, USA. AbstractBACKGROUND:The history of Chagas disease control in Peru and many other nations is marked by scattered and poorly documented vector control campaigns. The complexities of human migration and sporadic control campaigns complicate evaluation of the burden of Chagas disease and dynamics of Trypanosoma cruzi transmission. METHODOLOGY/PRINCIPAL FINDINGS:We conducted a cross-sectional serological and entomological study to evaluate temporal and spatial patterns of T. cruzi transmission in a peri-rural region of La Joya, Peru. We use a multivariate catalytic model and Bayesian methods to estimate incidence of infection over time and thereby elucidate the complex history of transmission in the area. Of 1,333 study participants, 101 (7.6%; 95% CI: 6.2-9.0%) were confirmed T. cruzi seropositive. Spatial clustering of parasitic infection was found in vector insects, but not in human cases. Expanded catalytic models suggest that transmission was interrupted in the study area in 1996 (95% credible interval: 1991-2000), with a resultant decline in the average annual incidence of infection from 0.9% (95% credible interval: 0.6-1.3%) to 0.1% (95% credible interval: 0.005-0.3%). Through a search of archival newspaper reports, we uncovered documentation of a 1995 vector control campaign, and thereby independently validated the model estimates. CONCLUSIONS/SIGNIFICANCE:High levels of T. cruzi transmission had been ongoing in peri-rural La Joya prior to interruption of parasite transmission through a little-documented vector control campaign in 1995. Despite the efficacy of the 1995 control campaign, T. cruzi was rapidly reemerging in vector populations in La Joya, emphasizing the need for continuing surveillance and control at the rural-urban interface. |
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| 9. | PLoS Negl Trop Dis. 2011 Feb 22;5(2):e852.A Latin American man with palpitations, dizziness, episodes of nonsustained ventricular tachycardia, and an apical aneurysm.Rassi A Jr, Rassi A, Franco-Paredes C.SourceSection of Cardiology, Anis Rassi Hospital, Goiânia, Brazil. arassijr@terra.com.br |
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| 10. | Protein Expr Purif. 2011 Apr;76(2):190-6. Epub 2010 Dec 4.Expression, purification and kinetic characterization of His-tagged glyceraldehyde-3-phosphate dehydrogenase from Trypanosoma cruzi.Cheleski J, Freitas RF, Wiggers HJ, Rocha JR, de Araújo AP, Montanari CA.SourceGrupo de Estudos em Química Medicinal de Produtos Naturais-NEQUIMED-PN, Instituto de Química de São Carlos, Universidade de São Paulo, São Carlos, SP, Brazil. AbstractTrypanosomes are flagellated protozoa responsible for serious parasitic diseases that have been classified by the World Health Organization as tropical sicknesses of major importance. One important drug target receiving considerable attention is the enzyme glyceraldehyde-3-phosphate dehydrogenase from the protozoan parasite Trypanosoma cruzi, the causative agent of Chagas disease (T. cruzi Glyceraldehyde-3-phosphate dehydrogenase (TcGAPDH); EC 1.2.1.12). TcGAPDH is a key enzyme in the glycolytic pathway of T. cruzi and catalyzes the oxidative phosphorylation of D-glyceraldehyde-3-phosphate (G3P) to 1,3-bisphosphoglycerate (1,3-BPG) coupled to the reduction of oxidized nicotinamide adenine dinucleotide, (NAD(+)) to NADH, the reduced form. Herein, we describe the cloning of the T. cruzi gene for TcGAPDH into the pET-28a(+) vector, its expression as a tagged protein in Escherichia coli, purification and kinetic characterization. The His(6)-tagged TcGAPDH was purified by affinity chromatography. Enzyme activity assays for the recombinant His(6)-TcGAPDH were carried out spectrophotometrically to determine the kinetic parameters. The apparent Michaelis-Menten constant (K(M)(app)) determined for D-glyceraldehyde-3-phosphate and NAD(+) were 352±21 and 272±25 μM, respectively, which were consistent with the values for the untagged enzyme reported in the literature. We have demonstrated by the use of Isothermal Titration Calorimetry (ITC) that this vector modification resulted in activity preserved for a higher period. We also report here the use of response surface methodology (RSM) to determine the region of optimal conditions for enzyme activity. A quadratic model was developed by RSM to describe the enzyme activity in terms of pH and temperature as independent variables. According to the RMS contour plots and variance analysis, the maximum enzyme activity was at 29.1°C and pH 8.6. Above 37°C, the enzyme activity starts to fall, which may be related to previous reports that the quaternary structure begins a process of disassembly. Copyright © 2010 Elsevier Inc. All rights reserved. |
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