What's new for 'Trypanosomatids' in PubMed

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Sent on Wednesday, 2010 Nov 03
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 - 10 of 19

1.	J Cytol. 2010 Jan;27(1):35-6. Leishmania life cycle images in the cutaneous cytologic smear of an immunocompetent patient. Zappacosta R, Claudi R, Magnasco S, Dell'osa E. Surgical Pathology Unit, Oncology and Neurosciences Department, Section of Cytopathology "G. d'Annunzio", University of Chieti-Pescara, Via Dei Vestini, Chieti, Italy. Abstract Cutaneous leishmania life cycle images on cytology smears are very rare. We report herein a gallery of cytologic images from a case of sporadic cutaneous leishmaniasis in a 61 year old man presenting with ulcerative skin lesion.
	PMID: 21042534 [PubMed - in process]
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2.	Ugeskr Laeger. 2010 Oct 18;172(42):2898-2899. [Leishmaniasis isolated to the larynx as cause of chronic laryngitis.] [Article in Danish] Kaltoft M, Munch-Petersen HR, Møller H. Porcelænshaven 4E. st. tv., 2000 Frederiksberg. mikkelkaltoft@dadlnet.dk. Abstract Mucosal leishmaniasis is uncommon outside Central and South America, where it is commonly caused by Leishmania (L.) braziliensis. We present a case of isolated laryngeal leishmaniasis detected in a 78-year-old male, who presented with chronic hoarseness. Histologic examination of biopsies taken from the larynx showed L. amastigotes. An L.-specific indirect fluorescent antibody test was positive. Polymerase chain reaction showed infection with L. donovani, L. infantum or L. tropica, species which do not normally cause isolated mucosal infection. This is the first reported case from Scandinavia.
	PMID: 21040662 [PubMed - as supplied by publisher]
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3.	Int J Health Geogr. 2010 Nov 1;9(1):57. [Epub ahead of print] The Atlas of human African trypanosomiasis: a contribution to global mapping of neglected tropical diseases. Simarro PP, Cecchi G, Paone M, Franco JR, Diarra A, Ruiz JA, Fevre EM, Courtin F, Mattioli RC, Jannin JG. Abstract ABSTRACT: BACKGROUND: Following World Health Assembly resolutions 50.36 in 1997 and 56.7 in 2003, the World Health Organization (WHO) committed itself to supporting human African trypanosomiasis (HAT)-endemic countries in their efforts to remove the disease as a public health problem. Mapping the distribution of HAT in time and space has a pivotal role to play if this objective is to be met. For this reason WHO launched the HAT Atlas initiative, jointly implemented with the Food and Agriculture Organization of the United Nations, in the framework of the Programme Against African Trypanosomosis. RESULTS: The distribution of HAT is presented for 23 out of 25 sub-Saharan countries having reported on the status of sleeping sickness in the period 2000 - 2009. For the two remaining countries, i.e. Angola and the Democratic Republic of the Congo, data processing is ongoing. Reports by National Sleeping Sickness Control Programmes (NSSCPs), Non-Governmental Organizations (NGOs) and Research Institutes were collated and the relevant epidemiological data were entered in a database, thus incorporating (i) the results of active screening of over 2.2 million people, and (ii) cases detected in health care facilities engaged in passive surveillance. A total of over 42 000 cases of HAT and 6 000 different localities were included in the database. Various sources of geographic coordinates were used to locate the villages of epidemiological interest. The resulting average mapping accuracy is estimated at 900 m. CONCLUSIONS: Full involvement of NSSCPs, NGOs and Research Institutes in building the Atlas of HAT contributes to the efficiency of the mapping process and it assures both the quality of the collated information and the accuracy of the outputs. Although efforts are still needed to reduce the number of undetected and unreported cases, the comprehensive, village-level mapping of HAT control activities over a ten-year period ensures a detailed and reliable representation of the known geographic distribution of the disease. Not only does the Atlas serve research and advocacy, but, more importantly, it provides crucial evidence and a valuable tool for making informed decisions to plan and monitor the control of sleeping sickness.
	PMID: 21040555 [PubMed - as supplied by publisher]
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4.	Zoonoses Public Health. 2010 Oct 12. doi: 10.1111/j.1863-2378.2010.01374.x. [Epub ahead of print] Genetic Diversity of Human Zoonotic Leishmaniasis in Iberian Peninsula. Cortes S, Chicharro C, Cruz I, Cristovão JM, Cañavate C, Campino L. Unidade de Leishmanioses, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, Lisboa, Portugal Servicio de Parasitologia, Centro Nacional de Microbiologia, Instituto de Salud Carlos III, Madrid, Spain. Abstract Leishmaniasis caused by Leishmania (Leishmania) infantum is a zoonotic disease endemic in South Europe, from Portugal to the Middle East. The aim of the present study was to investigate the genetic diversity of L. infantum parasites in Iberian Peninsula. Twenty-four L. infantum strains isolated from immunocompetent patients with leishmaniasis from several localities of Portugal and Spain were studied. The use of kinetoplast DNA-PCR-restriction fragment length polymorphism as a molecular marker revealed intra-specific variation. No association was found between genotype and clinical form of the disease or patients age group. Two main clusters were identified with this marker: (i) zymodeme MON-1 strains and (ii) non-MON-1 strains. However, no association was found between strains variability and geographical distribution suggesting that parasite populations of different regions in the Iberian Peninsula are homogenous. © 2010 Blackwell Verlag GmbH.
	PMID: 21040506 [PubMed - as supplied by publisher]
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5.	Chem Biol Drug Des. 2010 Oct 11. doi: 10.1111/j.1747-0285.2010.01035.x. [Epub ahead of print] Antimicrobial, Antimalarial, and Antileishmanial Activities of Mono- and Bis-quaternary Pyridinium Compounds. Bharate SB, Thompson CM. NIH COBRE Center for Structural and Functional Neuroscience, Department of Biomedical and Pharmaceutical Sciences, The University of Montana, Missoula, MT 59812, USA ATERIS Technologies LLC, 901 N Orange Street, Missoula, MT 59802, USA. Abstract Pyridinium-based oxime compounds have been utilized worldwide as antidotes following exposure to anticholinesterase agents. In the event of combined chemical and biological incident, it is of vital importance to know the ability of antidotes to provide additional protection against biological threats. This paper reports results of in vitro antimicrobial and antiprotozoal activities of a series of quaternary pyridinium oximes against a number of lower pathogenicity BSL-1 and 2 agents. In general, our compound panel had little to no antimicrobial action except for thiophene- and benzothiophene-substituted monoquaternary pyridinium compounds 21 and 24 that showed moderate antibacterial activity against Staphylococus aureus and methicillin-resistant S. aureus with IC(50) values ranging from 12.2 to 17.7 μg/mL. Compounds 21 and 24 also exhibited antileishmanial activity against Leishmania donovani with IC(50) values of 19 and 18 μg/mL, respectively. Another monoquaternary pyridinium compound with a bromobutyl side chain 17 showed antimalarial activity against both a chloroquine sensitive and resistant strains of Plasmodium falciparum with IC(50) values of 3.7 and 4.0 μg/mL, respectively. None of the bisquaternary pyridinium compounds showed antimicrobial or antiprotozoal activity. None of the compounds showed cytotoxic effects toward mammalian kidney fibroblasts. Results of this study indicate that the pyridinium compounds, some of which are already in use as antidotes, do not have significant antimicrobial and antiprotozoal activities and cannot be relied upon for additional protection in the event of combined chemical-biological incident. © 2010 John Wiley & Sons A/S.
	PMID: 21040494 [PubMed - as supplied by publisher]
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6.	Cell Microbiol. 2010 Oct 6. doi: 10.1111/j.1462-5822.2010.01537.x. [Epub ahead of print] Exosomes and other Microvesicles in Infection Biology: Organelles with Unanticipated Phenotypes. Silverman JM, Reiner NE. Departments of Medicine (Division of Infectious Diseases) and Microbiology and Immunology, University of British Columbia, and the Immunity and Infection Research Centre, Vancouver Coastal Health Research Institute, Vancouver, B.C, Canada. Abstract The release of exosomes and other microvesicles by diverse prokaryotic and eukaryotic cells and organisms was first appreciated early in the 20(th) century. The functional properties of these organelles, however, have only recently been the focus of rigorous investigation. In this review, we discuss the release of microvesicles of varying complexity by diverse microbial pathogens. This includes vesicle secretion by Gram negative bacteria, eukaryotic parasites of the kinetoplast lineage and opportunistic fungal pathogens of both the ascomycetes and basidiomycetes lineages. We also discuss vesicle release from mammalian cells brought about as a result of infection with bacteria, viruses and prions. In addition, we review the evidence showing that in their specific microenvironments, release of these organelles from diverse pathogens contributes to pathogenesis. Germane to this and based upon recent findings with Leishmania, we propose a model whereby exosome release by an intracellular pathogen serves as a general mechanism for effector molecule delivery from eukaryotic pathogen to host cell cytosol. These new findings linking exosomes and other microvesicles to infection biology have important implications for understanding the immune response to infection and for the design of research strategies aimed at the development of novel therapeutics and vaccines. © 2010 Blackwell Publishing Ltd.
	PMID: 21040357 [PubMed - as supplied by publisher]
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7.	Vet Dermatol. 2010 Oct 7. doi: 10.1111/j.1365-3164.2009.00863.x. [Epub ahead of print] Claw histopathology and parasitic load in natural cases of canine leishmaniosis associated with Leishmania infantum. Koutinas AF, Carlotti DN, Koutinas C, Papadogiannakis EI, Spanakos GK, Saridomichelakis MN. Department of Clinical Studies, Faculty of Veterinary Medicine, Aristotles University of Thessaloniki, Greece Veterinary Dermatology Clinic, Heliopolis, Bordeaux-Merignac, France Department of Veterinary Public Health, National School of Public Health, Athens, Greece Department of Parasitology, Entomology and Tropical Diseases, National School of Public Health, Athens, Greece Clinic of Medicine, School of Veterinary Medicine, University of Thessaly, Karditsa, Greece. Abstract Histological lesions and the presence of Leishmania spp. amastigotes in claw tissues were investigated in 40 dogs with leishmaniosis, with (16/40 - group A) or without (24/40 - group B) generalized onychogryphosis. Following euthanasia, the entire third phalanx with intact claw was amputated, formalin fixed, decalcified in a formic acid solution, embedded in paraffin, sectioned longitudinally and stained with haematoxylin and eosin, and acid orcein-Giemsa. Nested polymerase chain reaction (PCR) was used for the detection of Leishmania amastigotes. Lichenoid mononuclear infiltration (all dogs in group A, 21 of 24 dogs in group B), basal keratinocyte vacuolation (nine of 16 dogs in group A, 15 of 24 dogs in group B) and dermoepidermal clefting (13 of 16 dogs in group A, 18 of 24 dogs in group B) were the most prominent histopathological findings. There was no difference in the frequency and severity of these lesions between the two groups. Leishmania amastigotes could not be visualized in the dermis of any of the H&E sections, but their presence was demonstrated by nested PCR in three of 16 dogs in group A and two of 24 dogs in group B. However, the frequency of positive nested PCRs was not significantly different between the two groups. In conclusion, claw histopathology in symptomatic dogs with leishmaniosis, either with or without onychogryphosis is mainly characterized by mononuclear lichenoid dermatitis with or without interface dermatitis and dermoepidermal clefting, and is not accompanied by substantial local parasitism. © 2010 The Authors. Journal compilation © 2010 ESVD and ACVD.
	PMID: 21039983 [PubMed - as supplied by publisher]
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8.	Parasite Immunol. 2010 Nov;32(11-12):722-30. doi: 10.1111/j.1365-3024.2010.01237.x. Gentamicin-attenuated Leishmania infantum: cellular immunity production and protection of dogs against experimental canine lei shmaniasis. Daneshvar H, Molaei MM, Kamiabi H, Burchmore R, Hagan P, Stephen Phillips R. Medical School, University of Kerman Veterinary Medical School, Shahid Bahonar University of Kerman Department of Parasitology, Medical School, University of Kerman Sir Henry Wellcome Function Genomics Facility, institute of Biomedical and life Science Infection and Immunity, West Medical Building, University of Glasgow, Glasgow, UK. Abstract An attenuated line of Leishmania infantum (L. infantum H-line) has been established by culturing promastigotes in vitro under gentamicin pressure. Here, we show that L. infantum H-line induced significantly higher levels of IFN-γ and lower levels of IL-10 compared with those in dogs infected with L. infantum wild type (WT). Anti-Leishmania-specific total IgG, IgG1, and IgG2 antibodies were present in the serum of all infected dogs, with levels of IgG2 subclass highest in the sera of dogs inoculated with L. infantum H-line. Relatively high levels of IgG1 were found in the sera of dogs infected with L. infantum WT. Six of seven dogs immunized intradermally (i.d.) with the attenuated line later showed a positive skin test to leishmanin, whereas the dogs infected with L. infantum WT did not. No clinical abnormalities were observed, and no parasites found in the visceral organs of the dogs inoculated intravenously (i.v.) with L. infantum H-line over 24 months post-inoculation. Dogs which had been immunized with L. infantum H-line i.d. 12 months previously were protected against challenge with L. infantum WT. These data suggest that the L. infantum H-line was safe and induced a protection which is correlated with cellular immunity in dogs. © 2010 Blackwell Publishing Ltd.
	PMID: 21039612 [PubMed - in process]
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9.	South Med J. 2010 Oct 28. [Epub ahead of print] Visceral Leishmaniasis Mimicking Lymphoproliferative Disease. Kaziani K, Vadala C, Stasinopoulou P, Loverdos D, Samarkos M, Skoutelis A. 5th Department of Internal Medicine, Evangelismos Hospital, Athens, Greece.
	PMID: 21037515 [PubMed - as supplied by publisher]
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10.	J Immunol. 2010 Oct 29. [Epub ahead of print] IgG1 Is Pathogenic in Leishmania mexicana Infection. Chu N, Thomas BN, Patel SR, Buxbaum LU. Division of Infectious Diseases, Department of Medicine, University of Pennsylvania School of Medicine; Abstract There are >2 million new cases of leishmaniasis annually, and no effective vaccine has been developed to prevent infection. In murine infection, Leishmania mexicana, which lives intracellularly in host macrophages, has developed pathways to hijack host IgG to induce a suppressive IL-10 response through FcγRs, the cell-surface receptors for IgG. To guide vaccine development away from detrimental Ab responses, which can accompany attempts to induce cell-mediated immunity, it is crucial to know which isotypes of IgG are pathogenic in this infection. We found that IgG1 and IgG2a/c induce IL-10 from macrophages in vitro equally well but through different FcγR subtypes: IgG1 through FcγRIII and IgG2a/c through FcγRI primarily, but also through FcγRIII. In sharp contrast, mice lacking IgG1 develop earlier and stronger IgG2a/c, IgG3, and IgM responses to L. mexicana infection and yet are more resistant to the infection. Thus, IgG1, but not IgG2a/c or IgG3, is pathogenic in vivo, in agreement with prior studies indicating that FcγRIII is required for chronic disease. This calls into question the assumption that macrophages, which should secrete IL-10 in response to IgG1 and IgG2a/c immune complexes, are the most important source of IL-10 generated by IgG-FcγR engagement in L. mexicana infection. Further investigations are required to better determine the cell type responsible for this immunosuppressive FcγRIII-induced IL-10 pathway and whether IgG2a/c is protective.
	PMID: 21037092 [PubMed - as supplied by publisher]
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