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Sent on Tuesday, 2011 May 10Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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| PubMed Results |
| 1. | Rev Soc Bras Med Trop. 2011 Apr;44(2):254-6.American cutaneous leishmaniasis caused by Leishmania (Viannia) braziliensis resistant to meglumine antimoniate, but with good response to pentamidine: a case report.Pimentel MI, Baptista C, Rubin EF, Vasconcellos Ede C, Lyra MR, Salgueiro Mde M, Saheki MN, Rosalino CM, Madeira Mde F, Silva AF, Confort EM, Schubach Ade O.SourceLaboratório de Vigilância em Leishmanioses, Instituto de Pesquisa Clínica Evandro Chagas, Fundação Oswaldo Cruz, Rio de Janeiro, RJ. AbstractThis is a case report of a Brazilian soldier with cutaneous leishmaniasis. The lesion relapsed following two systemic treatments with meglumine antimoniate. The patient was treated with amphotericin B, which was interrupted due to poor tolerance. Following isolation of Leishmania sp., six intralesional infiltrations of meglumine antimoniate resulted in no response. Leishmania sp promastigotes were again isolated. The patient was submitted to intramuscular 4mg/kg pentamidine. Parasites from the first and second biopsies were identified as Leishmania (Viannia) braziliensis; those isolated from the first biopsy were more sensitive to meglumine antimoniate in vitro than those isolated from the second biopsy. No relapse was observed. |
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| 2. | PLoS One. 2011 Apr 28;6(4):e19000.Stage-Specific Pathways of Leishmania infantum chagasi Entry and Phagosome Maturation in Macrophages.Rodríguez NE, Gaur Dixit U, Allen LA, Wilson ME.SourceVeterans' Affairs Medical Center, Iowa City, Iowa, United States of America. AbstractThe life stages of Leishmania spp. include the infectious promastigote and the replicative intracellular amastigote. Each stage is phagocytosed by macrophages during the parasite life cycle. We previously showed that caveolae, a subset of cholesterol-rich membrane lipid rafts, facilitate uptake and intracellular survival of virulent promastigotes by macrophages, at least in part, by delaying parasitophorous vacuole (PV)-lysosome fusion. We hypothesized that amastigotes and promastigotes would differ in their route of macrophage entry and mechanism of PV maturation. Indeed, transient disruption of macrophage lipid rafts decreased the entry of promastigotes, but not amastigotes, into macrophages (P<0.001). Promastigote-containing PVs were positive for caveolin-1, and co-localized transiently with EEA-1 and Rab5 at 5 minutes. Amastigote-generated PVs lacked caveolin-1 but retained Rab5 and EEA-1 for at least 30 minutes or 2 hours, respectively. Coinciding with their conversion into amastigotes, the number of promastigote PVs positive for LAMP-1 increased from 20% at 1 hour, to 46% by 24 hours, (P<0.001, Chi square). In contrast, more than 80% of amastigote-initiated PVs were LAMP-1+ at both 1 and 24 hours. Furthermore, lipid raft disruption increased LAMP-1 recruitment to promastigote, but not to amastigote-containing compartments. Overall, our data showed that promastigotes enter macrophages through cholesterol-rich domains like caveolae to delay fusion with lysosomes. In contrast, amastigotes enter through a non-caveolae pathway, and their PVs rapidly fuse with late endosomes but prolong their association with early endosome markers. These results suggest a model in which promastigotes and amastigotes use different mechanisms to enter macrophages, modulate the kinetics of phagosome maturation, and facilitate their intracellular survival. |
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| 3. | Drug Des Devel Ther. 2011 Mar 16;5:175-81.Drug discovery and development for neglected diseases: the DNDi model.Chatelain E, Ioset JR.SourceDrugs for Neglected Diseases Initiative (DND i ), Geneva, Switzerland. AbstractNew models of drug discovery have been developed to overcome the lack of modern and effective drugs for neglected diseases such as human African trypanosomiasis (HAT; sleeping sickness), leishmaniasis, and Chagas disease, which have no financial viability for the pharmaceutical industry. With the purpose of combining the skills and research capacity in academia, pharmaceutical industry, and contract researchers, public-private partnerships or product development partnerships aim to create focused research consortia that address all aspects of drug discovery and development. These consortia not only emulate the projects within pharmaceutical and biotechnology industries, eg, identification and screening of libraries, medicinal chemistry, pharmacology and pharmacodynamics, formulation development, and manufacturing, but also use and strengthen existing capacity in disease-endemic countries, particularly for the conduct of clinical trials. The Drugs for Neglected Diseases initiative (DNDi) has adopted a model closely related to that of a virtual biotechnology company for the identification and optimization of drug leads. The application of this model to the development of drug candidates for the kinetoplastid infections of HAT, Chagas disease, and leishmaniasis has already led to the identification of new candidates issued from DNDi's own discovery pipeline. This demonstrates that the model DNDi has been implementing is working but its DNDi, neglected diseases sustainability remains to be proven. |
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| 4. | Medicina (B Aires). 2011;71(2):113-119.[Reactivity of GST-SAPA antigen of Trypanosoma cruzi against sera from patients with Chagas disease and leishmaniasis.] [Article in Spanish] Gil J, Cimino R, López Quiroga I, Cajal S, Acosta N, Juarez M, Zacca R, Orellana V, Krolewiecki A, Diosque P, Nasser J.SourceLaboratorio de Química Biológica y Biología Molecular, Facultad de Ciencias Naturales, Universidad Nacional de Salta (LQByBM). AbstractSerologic diagnosis of Trypanosoma cruzi infection is important due to the limited sensitivity of direct parasitologic methods for diagnosis in the indeterminate and chronic phases of disease. SAPA antigen has been used in several studies and has been shown to be a good marker for use in the diagnosis of T. cruzi infection. Chagas disease and leishmaniasis are endemic in northern Salta with overlapping zones of transmission, which frequently leads to T. cruzi-Leishmania spp. mixed infections. Diagnosis is complicated by the fact that there is significant cross-reactivity when non-specific antigens are used. We evaluated the reactivity of GST-SAPA antigen in the ELISA test (ELISA-SAPA) against sera from persons infected with T. cruzi (n = 154), leishmaniasis (n = 66), mixed infections (29), and healthy controls (n = 28) using commercial ELISA and IHA kits as reference tests. For ELISA-SAPA the sensitivity, specificity and kappa index were calculated for detection of T. cruzi infection. Among sera from patients infected with leishmaniasis, 30.5% of co-infections were detected. ELISA-SAPA sensitivity was 97.1% (confidence interval 95%: 94.5-99.9), specificity was 100% (confidence interval 95%: 99.4-100), and kappa index was 96% (confidence interval 95%: 93-99%), for detection of T. cruzi infection. Sensitivity, specificity and kappa indices have shown a high efficiency of ELISA-SAPA. |
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| 5. | Int J Antimicrob Agents. 2011 May 4. [Epub ahead of print]Antiprotozoal compounds: state of the art and new developments.Astelbauer F, Walochnik J.SourceInstitute of Specific Prophylaxis and Tropical Medicine, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Kinderspitalgasse 15, A-1090 Vienna, Austria. AbstractProtozoa can cause severe diseases, including malaria, leishmaniasis, Chagas disease, sleeping sickness and amoebiasis, all being responsible for morbidity and mortality particularly in tropical countries. To date there are no protective vaccines against any of these diseases, and many of the available drugs are old or elicit serious adverse reactions. Moreover, parasite resistance to existing drugs has become a serious problem. Owing to lack of financial returns, research in this field is of limited interest to pharmaceutical companies and largely depends on funding by public authorities. This article aims to provide a concise overview of the state-of-the-art treatment for the most important tropical protozoal infections as well as new approaches. Copyright © 2011 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. |
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| 6. | Skinmed. 2011 Mar-Apr;9(2):129-30.Pruritus as an unusual symptom in multiple piloleiomyoma.Sadeghian G, Ziaei H.SourceDisease and Leishmaniasis Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. sadeghian@sdlrc.mcui.a.ir AbstractA 30-year-old woman presented with multiple pruritic raised skin lesions at the proximal part of her left arm for the past 15 years. At the age of 15, the patient noticed red nodules accompanied with severe pruritus over the arm, which started to spread and involved the dorsal aspect of her scapula (Figure 1). They had been increasing in number during the past 15 years. There was no history of pain either spontaneously or in response to cold, tactile, or emotional stress, with no bleeding or oozing. There was no family history of similar skin lesions; however, she had a history of gynecologic problems for 10 years, and examination of her uterus showed uterine leiomyomas. The patient complained about severe pruritus. This symptom was exaggerated with sun exposure, cold, emotional stress, and rough cloths. It was so severe that it caused sleep disturbances. Clinical examination showed multiple pink and red nodules ranging from 5 mm to 20 mm over the above-described sites. The lesions were firm, smooth, not mobile, and nontender, with no pain on touch. Routine hematologic and biochemical investigations were normal. Kidney and pelvic ultrasonography showed myomatous uterus and normal kidneys. Microscopic examination of one of the nodules in hematoxylin and eosin-stained sections showed proliferation of smooth muscle cells with fascicular aspect in dermis. These cells had thin, elongated eel-like nuclei with blunt edges (Figure 2 and Figure 3). The diagnosis of leiomyoma was made and the patient was referred for surgical excision. Due to the extension and site of the lesions, the plastic surgeon did not recommend surgical procedure and the patient was treated with an antihistamine (loratadine 10 mg/d). |
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| 7. | Parasitol Res. 2011 Feb;108(2):459-66. Epub 2010 Oct 1.Sequencing and analysis of chromosomal extremities of Trypanosoma rangeli in comparison with Trypanosoma cruzi lineages.Cabrine-Santos M, Ramírez LE, Lages-Silva E, de Souza BF, Pedrosa AL.SourceDiscipline of Parasitology, Department of Biological Sciences, Federal University of Triângulo Mineiro, 38025-180, Uberaba, Minas Gerais, Brazil. AbstractThe aim of this study was to investigate the genetic variability of sequences present in the chromosome ends of Trypanosoma rangeli strains defined by the presence (+) or absence (-) of KP1 minicircles, and to compare the mean terminal restriction fragment (TRF) lengths to those of Trypanosoma cruzi populations representative of groups TcI, TcII, TcIV, and TcVI. Southern blots containing RsaI-digested genomic DNA of T. rangeli KP1(+) strains, T. rangeli KP1(-) strains, and T. cruzi strains were probed with the previously described subtelomeric sequences (170 bp) of T. rangeli and with telomeric hexamer repeats. Mean TRF length analysis showed that the chromosome ends of T. rangeli are distinctly organized, with TRFs ranging from 1.3 to 9 kb for KP1(+) strains and from 0.3 to 5.0 kb for KP1(-) strains. In T. cruzi, TRF length ranged from 0.2 to 9 kb and no association with the genotype of the parasite could be established. Sequence analysis of the 170-bp amplicons revealed the occurrence of sequence polymorphisms in the subtelomeric region between and within KP1(+) and KP1(-) strains. The GTT triplet was detected in all KP1(+) strains, except for strain Cas4, but not in any of the KP1(-) strains. The dendrogram constructed by alignment of all T. rangeli strains showed the division into two main groups, mainly related to the presence or absence of the KP1 minicircle. In conclusion, the present results extend the genotype differences demonstrated by kDNA and karyotype analysis in T. rangeli to the chromosome ends of the parasite. |
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