Friday, August 7, 2009

What's new for 'Trypanosomatids' in PubMed

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Search kinetoplastids OR kinetoplastid OR Kinetoplastida OR "trypanosoma brucei" OR leishmania OR brucei OR leishmaniasis OR "African trypanosomiasis"
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PubMed Results
Items 1 -6 of 6

1: J Trop Pediatr. 2009 Aug 5. [Epub ahead of print]Click here to read

Successful Treatment of Childhood Cutaneous Leishmaniasis with Liposomal Amphotericin B: Report of Two Cases.

Hospital La Paz, Department of Pediatric Infectious Diseases, Madrid, Spain.

Treatment of cutaneous leishmaniasis is sometimes difficult. No single ideal therapy has yet been identified and some of the drugs that are currently used are associated with significant toxicity. We present two cases of cutaneous leishmaniasis in children, one caused by Leishmania infantum and the other by Leishmania braziliensis. Both of them were successfully treated with intravenous liposomal amphotericin B.

PMID: 19656844 [PubMed - as supplied by publisher]

2: Protist. 2009 Aug 3. [Epub ahead of print]Click here to read

Cell Morphogenesis of Trypanosoma brucei Requires the Paralogous, Differentially Expressed Calpain-related Proteins CAP5.5 and CAP5.5V.

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

Proteins from the calpain super-family are involved in developmentally- and environmentally-regulated re-modelling of the eukaryotic cytoskeleton and the dynamic organisation of signal transduction cascades. In trypanosomatid parasites, calpain-related gene families are unusually large, but we have little insight into the functional roles played by these molecules during trypanosomatid lifecycles. Here we report that CAP5.5, a cytoskeletal calpain-related protein subject to strict stage-specific expression in the sleeping sickness parasite Trypanosoma brucei, is essential and required for correct cell morphogenesis of procyclic (tsetse mid-gut stage) T. brucei. Striking consequences of CAP5.5 RNA interference are the loss of protein from the posterior cell-end, organelle mis-positioning giving rise to aberrant cytokinesis, and disorganisation of the sub-pellicular microtubules that define trypanosome cell shape. We further report that the stage-specificity of CAP5.5 expression can be explained by the presence of a paralogue, CAP5.5V, which is required for cell morphogenesis in bloodstream T. brucei; RNAi against this paralogous protein results in a qualitatively similar phenotype to that described for procyclic CAP5.5 RNAi mutants. By comparison to recently described phenotypes for other procyclic trypanosome RNAi mutants, likely functions for CAP5.5 and CAP5.5V are discussed.

PMID: 19656721 [PubMed - as supplied by publisher]

3: Vet Parasitol. 2009 Jul 19. [Epub ahead of print]Click here to read

Different isolates from Leishmania braziliensis complex induce distinct histopathological features in a murine model of infection.

Laboratório de Biologia Molecular, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, Brazil.

The aim of this study was to evaluate the histopathological features in tissues of mice infected by human isolates (I, II, and III) or the reference M2903 strain of Leishmania braziliensis complex. BALB/c and C57Bl/6 mice were infected in the hind footpad with 10(6) stationary-phase promastigotes of L. braziliensis complex. The evolution of lesions was observed for 10 weeks and the animals were then euthanized and liver, spleen and popliteal lymph nodes were collected. Tissues were stained with hematoxylin and eosin and analyzed by immunohistochemistry assay. Increased thickness of infected footpads was observed in all animals, lesions were nodular and non-ulcerated. Mice infected with isolate I presented inflammatory infiltrates consisting predominantly of mononuclear cells in all tissues examined, and also a great number of megakaryocytes, compared with other isolates. Infection with isolate II led to an infected footpad enlargement not seen in other isolates. In addition, mononuclear infiltrates in the liver and hemosiderin in spleen were noted. Conversely, mice infected with either isolate III or M2903 strain only showed an increased number of megakaryocytes in spleen. All tissues examined had detectable amastigote forms of Leishmania by immunohistochemistry in all groups. Taking together, our results showed an unforeseen behavior of different isolates of L. braziliensis complex that led to diverse pathological findings.

PMID: 19656631 [PubMed - as supplied by publisher]

4: J Med Entomol. 2009 May;46(3):708-11.LinkOut

Presence of Rhodnius ecuadoriensis in sylvatic habitats in the southern highlands (Loja Province) of Ecuador.

Tropical Disease Institute, Biomedical Sciences Department, College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA. grijalva@ohiou.edu

The main vectors of Chagas disease in Ecuador are Triatoma dimidiata and Rhodnius ecuadoriensis. The latter species occupies domestic and peridomestic habitats, as well as sylvatic ecotopes--particularly associated with Phytelephas aequatorialis palm trees--in the western coastal region of Ecuador. In the southern highlands, however, such palm tree habitats are uncommon, and sylvatic populations of R. ecuadoriensis have not previously been reported to date. This study was carried out in five rural communities in Loja Province in southern Ecuador, where manual triatomine searches were conducted in various sylvatic habitats. A total of 81 squirrel nests (Sciurus stramineus) and > 200 bird nests and other habitats were searched. One hundred three R. ecuadoriensis individuals were found in 11 squirrel nests (infestation index = 13.6%, density = 2 bugs per nest searched, crowding = 9.5 bugs per infested nest, colonization index = 72.7% of infested nests with nymphs). No triatomines were found in bird nests or other sylvatic habitats. The presence of sylvatic R. ecuadoriensis in the southern highlands of Ecuador has important implications for the long-term control of Chagas disease in the region because of the possibility of reinfestation of dwellings after insecticide-based control interventions.

PMID: 19496445 [PubMed - indexed for MEDLINE]

5: PLoS One. 2009;4(5):e5564. Epub 2009 May 15.Click here to read Click here to read References for this PMC Article, Free in PMC, LinkOut

Discovery of mating in the major African livestock pathogen Trypanosoma congolense.

Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow Biomedical Research Centre, Glasgow, United Kingdom. lm78y@udcf.gla.ac.uk

The protozoan parasite, Trypanosoma congolense, is one of the most economically important pathogens of livestock in Africa and, through its impact on cattle health and productivity, has a significant effect on human health and well being. Despite the importance of this parasite our knowledge of some of the fundamental biological processes is limited. For example, it is unknown whether mating takes place. In this paper we have taken a population genetics based approach to address this question. The availability of genome sequence of the parasite allowed us to identify polymorphic microsatellite markers, which were used to genotype T. congolense isolates from livestock in a discrete geographical area of The Gambia. The data showed a high level of diversity with a large number of distinct genotypes, but a deficit in heterozygotes. Further analysis identified cryptic genetic subdivision into four sub-populations. In one of these, parasite genotypic diversity could only be explained by the occurrence of frequent mating in T. congolense. These data are completely inconsistent with previous suggestions that the parasite expands asexually in the absence of mating. The discovery of mating in this species of trypanosome has significant consequences for the spread of critical traits, such as drug resistance, as well as for fundamental aspects of the biology and epidemiology of this neglected but economically important pathogen.

PMID: 19440370 [PubMed - indexed for MEDLINE]

PMCID: PMC2679202

6: J Biol Chem. 2009 Jun 26;284(26):17404-10. Epub 2009 May 1.Click here to read LinkOut

A new sialidase mechanism: bacteriophage K1F endo-sialidase is an inverting glycosidase.

Department of Chemistry, University of British Columbia, Vancouver, British Columbia V6T 1Z1.

Bacteriophages specific for Escherichia coli K1 express a tailspike protein that degrades the polysialic acid coat of E. coli K1 that is essential for bacteriophage infection. This enzyme is specific for polysialic acid and is a member of a family of endo-sialidases. This family is unusual because all other previously reported sialidases outside of this family are exo- or trans-sialidases. The recently determined structure of an endo-sialidase derived from bacteriophage K1F (endoNF) revealed an active site that lacks a number of the residues that are conserved in other sialidases, implying a new, endo-sialidase-specific catalytic mechanism. Using synthetic trifluoromethylumbelliferyl oligosialoside substrates, kinetic parameters for hydrolysis at a single cleavage site were determined. Measurement of kcat/Km at a series of pH values revealed a dependence on a single protonated group of pKa 5. Mutation of a putative active site acidic residue, E581A, resulted in complete loss of sialidase activity. Direct 1H NMR analysis of the hydrolysis of trifluoromethylumbelliferyl sialotrioside revealed that endoNF is an inverting sialidase. All other wild type sialidases previously reported are retaining glycosidases, implying a new mechanism of sialidase action specific to this family of endo-sialidases.

PMID: 19411257 [PubMed - indexed for MEDLINE]

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