Tuesday, January 12, 2010

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 -10 of 12

1. Arch Dermatol Res. 2010 Jan 9. [Epub ahead of print]

Purified proteins from leishmania amastigotes-induced delayed type hypersensitivity reactions and remission of collagen-induced arthritis in animal models.

O'Daly JA, Gleason JP, Peña G, Colorado I.

Astralis LTD., 75 Passaic Ave., Fairfield, NJ, 07004, USA, joseodaly@aol.com.

A treatment preparation composed of purified Leishmania (L) antigenic fractions (AS210) induced linear delayed type hypersensitivity (DTH) reactions over a 1-40 mug dose range, in guinea pigs. When a DBA-1 mouse collagen induced arthritis (CIA) model was used to compare AS210 treatment against: a polyvalent vaccine (AS110-1), a monovalent vaccine (AS110-2) and placebo, the AS210 treated mice had the least amount of forepaw inflammation and the lowest mean arthritis scores (MAS). When MAS for day(s) 1-40 were analyzed using one way ANOVA, statistically significant (P < 0.05) differences were seen for the following study groups: PBS versus Dexamethasone and PBS versus AS210. Subsequently, the ANOVA analysis results were corroborated by the Mann-Whitney test: analysis of the first group (P < 0.001) and analysis of the second group (P < 0.001). Comparison between dexamethasone and AS210 at different time intervals by Mann-Whitney test were as follows: day 0-day 5 both treatments had equal values (P = 1.00), from day-7 to 20 AS210 treatment had lower MAS values than dexamethasone (P = 0.037), and from day-21 to 30, AS210 MAS were similar to dexamethasone values (P = 0.319). No statistical difference was observed between AS110-1, AS110-2, and placebo groups.

PMID: 20063004 [PubMed - as supplied by publisher]
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2. PLoS One. 2010 Jan 7;5(1):e8628.

No Gold Standard Estimation of the Sensitivity and Specificity of Two Molecular Diagnostic Protocols for Trypanosoma brucei spp. in Western Kenya.

de Clare Bronsvoort BM, von Wissmann B, Fèvre EM, Handel IG, Picozzi K, Welburn SC.

The Roslin Institute and The Royal (Dick) School of Veterinary Studies, University of Edinburgh, Roslin, Midlothian, United Kingdom.

African animal trypanosomiasis is caused by a range of tsetse transmitted protozoan parasites includingTrypanosoma vivax, Trypanosoma congolense and Trypansoma brucei. In Western Kenya and other parts of East Africa two subspecies of T. brucei, T.b. brucei and the zoonoticT.b. rhodesiense, co-circulate in livestock. A range of polymerase chain reactions (PCR) have been developed as important molecular diagnostic tools for epidemiological investigations of T. brucei s.l. in the animal reservoir and of its zoonotic potential. Quantification of the relative performance of different diagnostic PCRs is essential to ensure comparability of studies. This paper describes an evaluation of two diagnostic test systems for T. brucei using a T. brucei s.l. specific PCR [1] and a single nested PCR targeting the Internal Transcribed Spacer (ITS) regions of trypanosome ribosomal DNA [2]. A Bayesian formulation of the Hui-Walter latent class model was employed to estimate their test performance in the absence of a gold standard test for detecting T.brucei s.l. infections in ear-vein blood samples from cattle, pig, sheep and goat populations in Western Kenya, stored on Whatman FTA cards. The results indicate that the system employing the T. brucei s.l. specific PCR (Se(1) = 0.760) had a higher sensitivity than the ITS-PCR (Se(2) = 0.640); both have high specificity (Sp(1) = 0.998; Sp(2) = 0.997). The true prevalences for livestock populations were estimated (p(cattle) = 0.091, p(pigs) = 0.066, p(goats) = 0.005(,) p(sheep) = 0.006), taking into account the uncertainties in the specificity and sensitivity of the two test systems. Implications of test performance include the required survey sample size; due to its higher sensitivity and specificity, the T. brucei s.l. specific PCR requires a consistently smaller sample size than the ITS-PCR for the detection of T. brucei s.l. However the ITS-PCR is able to simultaneously screen samples for other pathogenic trypanosomes and may thus be, overall, a better choice of test in multi-organism studies.

PMID: 20062795 [PubMed - in process]
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3. Indian J Dermatol Venereol Leprol. 2010 Jan-Feb;76(1):85.

Lupoid cutaneous leishmaniasis: a report of 16 cases.

Ul Bari A, Raza N.

Department of Dermatology, Combined Military Hospital, Peshawar, Faisal, Pakistan.

BACKGROUND: Lupoid cutaneous leishmaniasis (CL) is known as the chronic form of CL. However, keeping its clinical presentation in view, there is a need to revisit this form of disease. AIMS: To redefine/describe lupoid CL in view of clinical features. METHODS: It was a case series seen in Muzaffarabad (Pakistan) from Jan 2006 to May 2008. All patients clinically suggestive and consistent with laboratory diagnosis of CL were registered. Patients of all age groups and either sex having cutaneous lesions resembling lupus vulgaris or lupus erythematosus on the face or elsewhere were included in the study. Those having chronic fluctuating/relapsing course or scarring within the lesions were also included. Various demographic features of the patients and clinical patterns were recorded. Descriptive statistics were used for analysis. RESULTS: Of 254 registered patients of CL, 16 (6.3%) were diagnosed as lupoid CL. None of the patients had scarred lesions. Age ranged from 38 to 75 (55 + 15.11) years and duration of lesions varied from 4 to 32 (14.25 + 07.59) weeks. All patients had lesions over the face. Thirteen (81.25%) had a large solitary plaque extending over the nose and a large part of the cheeks and three (18.75%) had multiple lesions. Lesions were central/nasal in two (12.5%), unilateral/asymmetrical in four (25%) and bilateral/symmetrical in 10 (62.5%). Morphological patterns included erythematous/infiltrated (7), psoriasiform (6), ulcerated/crusted (2) and Discoid lupus erythematosus (DLE)[G1] like (1). CONCLUSION: Lupoid CL is not strictly a chronic form of disease, which presents on the face from the very onset and shows no scarring or recurrence.

PMID: 20061750 [PubMed - in process]
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4. Saudi J Kidney Dis Transpl. 2010 Jan-Feb;21(1):105-8.

Visceral leishmaniasis in a renal transplant recipient treated with allopurinol.

Harzallah K, Belhadj R, Jemli B, Haloues M, Berraies N, Gargouri S, Hmida J, Battikh R, Manaa J.

Unity of Organ Transplantation, Military Hospital, Tunis, Tunisia.

Leishmaniasis is an infection caused by a protozoan parasite belonging to the genus Leishmania and transmitted by the Phlebotomus sandfly. We report a case of visceral leishmaniasis in a 49-year-old male renal transplant recipient, a resident of the western part of Tunisia, which is an endemic zone for the disease. Just before and after the transplantation, the patient resided in Tunis, which is non-endemic for leishmaniasis. Visceral leishmaniasis occurred eight years after renal transplantation, and the clinical picture was characterized by fever and pancytopenia. Leish-maniae were detected by bone marrow aspiration. Pentavalent antimonal was used for 28 days and was substituted by allopurinol (20 mg/kg per day). One year after the infection, the patient remains totally asymptomatic. Our report suggests that visceral leishmaniasis may complicate the clinical course of organ transplantation and can be fatal, particularly when untreated. Relapses may occur after completion of the apparently effective treatment. Allopurinol could be a solution to avoid these relapses.

PMID: 20061702 [PubMed - in process]
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5. Comp Immunol Microbiol Infect Dis. 2010 Jan 8. [Epub ahead of print]

Comparison between three adjuvant s for a vaccine against canine leishmaniasis: In vitro evaluation of macrophage killing ability.

Trotta T, Fasanella A, Scaltrito D, Gradoni L, Mitolo V, Brandonisio O, Acquafredda A, Panaro MA.

Dipartimento di Scienze Biomediche, Sezione di Anatomia Umana, University of Foggia, Ospedali Riuniti, Viale L. Pinto, 71100 Foggia, Italy.

The aim of this study was to evaluate, in terms of dog macrophage killing ability in vitro, a vaccine based on Leishmania infantum promastigote soluble antigen (LSA) formulated with three different adjuvants (BCG, AdjuPrime, MPL/TDM/CWS). A significant increase of the macrophage killing ability was observed in dogs vaccinated with LSA+MPL/TDM/CWS after 1 month from vaccination. A similar increase of macrophage parasitocidal ability was present only after 5 months in dogs vaccinated with LSA+BCG or LSA+AdjuPrime. In all dogs the augmented killing percentage was still present after 12 months from vaccination. Therefore, in particular LSA+MPL/TDM/CWS vaccine seems promising for further studies in dogs. Copyright © 2009 Elsevier Ltd. All rights reserved.

PMID: 20061026 [PubMed - as supplied by publisher]
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6. Arch Biochem Biophys. 2010 Jan 7. [Epub ahead of print]

Role of C-terminal acidic cluster in stabilization of hem e spin state of ascorbate peroxidase from Leishmania major.

Yadav RK, Dolai S, Pal S, Adak S.

Division of Structural Biology and Bio-informatics, Indian Institute of Chemical Biology, Council of Scientific and Industrial Research, 4, Raja S.C. Mullick Road, Kolkata - 700 032, India.

Architecture of hemoprotein is solely responsible for different nature of heme coordination. Here we report that substitution of the acidic surface residue Glu226 to Ala in ascorbate peroxidase from L. major alters the 5 coordinate high spin (5cHS) to a 6 coordinate low spin (6cLS) form at pH 7.5. Using UV-Visible spectrophotometry, we show that the sixth ligand of heme in Glu226Ala at pH 7.5 is hydroxo. When the pH is decreased to 5.5, a new species of Glu226Ala appeared that had a spectrum characteristic of a 6cHS derivative. Stopped flow spectrophotometric techniques revealed that characteristics of compound I was not seen in the Glu226Ala in presence of H(2)O(2). Similarly guaiacol, ascorbate and ferrocytochrome c oxidation rate was 10(3) orders less for the Glu226Ala mutants compared to the wild type. These data suggested that surface acidic residue Glu226 might play role in proper maintenance of active site conformation. Copyright © 2010. Published by Elsevier Inc.

PMID: 20060805 [PubMed - as supplied by publisher]
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7. Vet Parasitol. 2009 Dec 24. [Epub ahead of print]

Toxoplasma gondii and Leishmania spp. infection in captive crab-eating foxes, Cerdocyon thous (Carnivora, Canidae) from Brazil.

Catenacci LS, Griese J, da Silva RC, Langoni H.

Instituto de Estudos Socioambientais do sul da Bahia (IESB), Rua Major Homem d'El Rey, 147 Cidade Nova, Ilhéus, CEP 45652-180, BA, Brazil.

The zoonoses toxoplasmosis and leishmaniasis are important worldwide and also affect wild animals. Thus, the present study aimed to assess the prevalence of Leishmania spp. and Toxoplasma gondii antibodies in 52 serum samples from captive crab-eating foxes (Cerdocyon thous) kept in 17 zoos in São Paulo State, Brazil. Modified agglutination test (MAT, for toxoplasmosis) and indirect fluorescent antibody test (IFAT, for toxoplasmosis and leishmaniasis) were employed with heterologous anti-dog immunoglobulin. Antibodies to T. gondii were found in 19.2% animals, with an almost perfect concordance (kappa=0.86; standard error=9.31%; CI95%=68.25-104.76%; P<0.0001) and a strong correlation coefficient (rs=0.87; P<0.0001), which allows the use of heterologous anti-dog immunoglobulin to perform IFAT for toxoplasmosis in crab-eating foxes. No sample was positive for Leishmania spp. Toxoplasmosis infection occurs in wild animals from the studied Brazilian zoos, which indicates a probable environmental contamination, highlighting the importance of appropriate zoo management and the action of the parasite as a sentinel to human infection. Copyright © 2009 Elsevier B.V. All rights reserved.

PMID: 20060648 [PubMed - as supplied by publisher]
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8. Parasitol Int. 2010 Jan 5. [Epub ahead of print]

Histopathology, humoral and cellular immune response in the murine model of Leishmania (Viannia) shawi.

Passero LF, Marques C, Vale-Gato I, Corbett CE, Laurenti MD, Santos-Gomes G.

Laboratorio Patologia de Moléstias Infecciosas, Faculdade de Medicina da Universidade de São Paulo, Brazil. Av. Dr. Arnaldo, 455, São Paulo, Brazil.

Leishmania (Viannia) shawi was recently characterized and few studies concerning modifications in cellular and humoral immune responses in experimental leishmaniasis have been conducted. In this work, immunopathological changes induced by L. shawi in chronically infected BALB/c mice were investigated. Infected BALB/c mice developed increased lesion size associated with strong inflammatory infiltrate diffusely distributed in the dermis, with highly infected macrophages. The humoral immune response was predominantly directed toward the IgG1 isotype. The functional activity of CD4(+) and CD8(+) T cells showed significantly increased TNF-alpha mRNA levels associated with reduced IFN-gamma expression by CD4(+) T cells and the double negative (dn) CD4CD8 cell subset. High IL-4 levels expressed by CD8(+) T cells and dnCD4CD8 and TGF-beta by CD4(+) and CD8(+) T cells were detected, while IL-10 was highly expressed by all three cell subpopulations. Taken together, these results show an evident imbalance between TNF-alpha and IFN-gamma that is unfavorable to amastigote replication control. Furthermore, L. shawi seems to regulate different cell populations to express deactivating cytokines to avoid its own destruction. This study indicates BALB/c mice as a potentially good experimental model for further studies on American cutaneous leishmaniasis caused by L. shawi. Copyright © 2009. Published by Elsevier Ireland Ltd.

PMID: 20060062 [PubMed - as supplied by publisher]
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9. Free Radic Biol Med. 2009 Nov 15;47(10):1408-13. Epub 2009 Aug 18.

The effect of alpha-tocopherol transfer protein gene disruption on Trypanosoma congolense infection in mice.

Herbas MS, Thekisoe OM, Inoue N, Xuan X, Arai H, Suzuki H.

Research Unit for Functional Genomics, National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Nishi 2-13, Inada, Obihiro 080-8555, Japan.

At present 15 to 20 million people are estimated to be infected with pathogenic trypanosome parasites worldwide, mainly in developing countries. There are a number of factors that affect the severity of trypanosomiasis, including the nutritional status of the host. However, the relationship between micronutrient levels and trypanosomiasis outcome has yet to be reported in detail. Here, we demonstrate that the inhibition of alpha-tocopherol transfer protein, a determinant of the vitamin E concentration in host circulation, confers resistance to Trypanosoma congolense infection, evidently owing to oxidative damage to parasite DNA. These results suggest that transient inhibition of alpha-tocopherol transfer gene activity could possibly be exploited as a strategy for both the prevention and the treatment of trypanosomiasis.

PMID: 19695323 [PubMed - indexed for MEDLINE]
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Publication Types:

  • Research Support, Non-U.S. Gov't

MeSH Terms:

  • Animals
  • Antioxidants/metabolism
  • Carrier Proteins/antagonists & inhibitors
  • Carrier Proteins/genetics*
  • Disease Models, Animal
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Oxidative Stress
  • Reactive Oxygen Species/metabolism
  • Trypanosoma congolense/immunology*
  • Trypanosomiasis, African/genetics*
  • Trypanosomiasis, African/immunology
  • Trypanosomiasis, African/veterinary
  • Vitamin E/pharmacology
  • Vitamin E Deficiency/genetics
  • Vitamin E Deficiency/immunology

Substances:

  • Antioxidants
  • Carrier Proteins
  • Reactive Oxygen Species
  • alpha-tocopherol transfer protein
  • Vitamin E
10. Free Radic Biol Med. 2009 Nov 15;47(10):1414-21. Epub 2009 Aug 14.

Trypanosoma cruzi infection disturbs mitochondrial membrane potential and ROS production rate in cardiomyocytes.

Gupta S, Bhatia V, Wen JJ, Wu Y, Huang MH, Garg NJ.

Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.

In this study, we investigated the role of Trypanosoma cruzi invasion and inflammatory processes in reactive oxygen species (ROS) production in a mouse atrial cardiomyocyte line (HL-1) and primary adult rat ventricular cardiomyocytes. Cardiomyocytes were incubated with T. cruzi (Tc) trypomastigotes, Tc lysate (TcTL), or Tc secreted proteins (TcSP) for 0-72 h, and ROS were measured by amplex red assay. Cardiomyocytes infected by T. cruzi (but not those incubated with TcTL or TcSP) exhibited a linear increase in ROS production for 2-48 h postinfection (max 18-fold increase), which was further enhanced by recombinant cytokines (IL-1beta, TNF-alpha, and IFN-gamma). We observed no increase in NADPH oxidase, xanthine oxidase, or myeloperoxidase activity, and specific inhibitors of these enzymes did not block the increased rate of ROS production in infected cardiomyocytes. Instead, the mitochondrial membrane potential was perturbed and resulted in inefficient electron transport chain (ETC) activity and enhanced electron leakage and ROS formation in infected cardiomyocytes. HL-1 rho (rho) cardiomyocytes lacked a functional ETC and exhibited no increase in ROS formation in response to T. cruzi. Together, these results demonstrate that invasion by T. cruzi and an inflammatory milieu affect mitochondrial integrity and contribute to electron transport chain inefficiency and ROS production in cardiomyocytes.

PMCID: PMC2767388 [Available on 2010/11/15]

PMID: 19686837 [PubMed - indexed for MEDLINE]
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Publication Types:

  • Research Support, N.I.H., Extramural

MeSH Terms:

  • Animals
  • Cells, Cultured
  • Fluorescent Dyes/chemistry
  • Mice
  • Mitochondrial Membranes/drug effects
  • Mitochondrial Membranes/immunology*
  • Myocytes, Cardiac/drug effects
  • Myocytes, Cardiac/immunology*
  • Rats
  • Reactive Oxygen Species/immunology*
  • Trypanocidal Agents/pharmacology
  • Trypanosoma cruzi/drug effects
  • Trypanosoma cruzi/immunology
  • Trypanosoma cruzi/isolation & purification*

Substances:

  • Fluorescent Dyes
  • Reactive Oxygen Species
  • Trypanocidal Agents

Grant Support:

  • AI054578/AI/NIAID NIH HHS/United States

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