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Biblioteca (s) : |
INIA La Estanzuela. |
Fecha : |
02/03/2017 |
Actualizado : |
07/03/2017 |
Autor : |
GARCIA, J.P; GIANNITTI, F.; FINNIE, J.W.; MANAVIS, J. .; BEINGESSER, J.; ADAMS ,V.; ROOD, J.I.; UZAL, F.A. |
Afiliación : |
FEDERICO GIANNITTI, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay. |
Título : |
Comparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives. |
Fecha de publicación : |
2015 |
Fuente / Imprenta : |
Veterinary Pathology, 2015, v.52.n.6. p.1250-1253, 2015. |
Idioma : |
Inglés |
Contenido : |
Abstract
Clostridium perfringens type D causes enterotoxemia in sheep and goats. The disease is mediated by epsilon toxin (ETX), which affects the cerebrovascular endothelium, increasing vascular permeability and leading to cerebral edema. In the present study, we compared the distribution and severity of the cerebrovascular changes induced in lambs by C. perfringens type D strain CN1020, its isogenic etx null mutant, and the ETX-producing complemented mutant. We also applied histochemical and immunohistochemical markers to further characterize the brain lesions induced by ETX. Both ETX-producing strains induced extensive cerebrovascular damage that did not differ significantly between each other in nature, neuroanatomic distribution, or severity. By contrast, lambs inoculated with the etx mutant or sterile, nontoxic culture medium did not develop detectable brain lesions, confirming that the neuropathologic effects observed in these infections are dependent on ETX production. Lambs treated with the wild-type and complemented strains showed perivascular and mural vascular edema, as well as serum albumin extravasation, particularly severe in the cerebral white matter, midbrain, medulla oblongata, and cerebellum. Brains of animals inoculated with the ETX-producing strains showed decreased expression of glial fibrillary acidic protein and increased expression of aquaporin-4 in the end-feet processes of the astrocytes around blood vessels. Early axonal injury was demonstrated with anti?amyloid precursor protein immunohistochemistry. Perivascular accumulation of macrophages/microglia with intracytoplasmic albumin globules was also observed in these animals. This study demonstrates that ETX is responsible for the major cerebrovascular changes in C. perfringens type D?induced disease. MenosAbstract
Clostridium perfringens type D causes enterotoxemia in sheep and goats. The disease is mediated by epsilon toxin (ETX), which affects the cerebrovascular endothelium, increasing vascular permeability and leading to cerebral edema. In the present study, we compared the distribution and severity of the cerebrovascular changes induced in lambs by C. perfringens type D strain CN1020, its isogenic etx null mutant, and the ETX-producing complemented mutant. We also applied histochemical and immunohistochemical markers to further characterize the brain lesions induced by ETX. Both ETX-producing strains induced extensive cerebrovascular damage that did not differ significantly between each other in nature, neuroanatomic distribution, or severity. By contrast, lambs inoculated with the etx mutant or sterile, nontoxic culture medium did not develop detectable brain lesions, confirming that the neuropathologic effects observed in these infections are dependent on ETX production. Lambs treated with the wild-type and complemented strains showed perivascular and mural vascular edema, as well as serum albumin extravasation, particularly severe in the cerebral white matter, midbrain, medulla oblongata, and cerebellum. Brains of animals inoculated with the ETX-producing strains showed decreased expression of glial fibrillary acidic protein and increased expression of aquaporin-4 in the end-feet processes of the astrocytes around blood vessels. Early axonal injury was demonstrated wi... Presentar Todo |
Thesagro : |
ENFERMEDADES DE LOS ANIMALES. |
Asunto categoría : |
-- |
Marc : |
LEADER 02512naa a2200217 a 4500 001 1056750 005 2017-03-07 008 2015 bl uuuu u00u1 u #d 100 1 $aGARCIA, J.P 245 $aComparative Neuropathology of Ovine Enterotoxemia Produced by Clostridium perfringens Type D Wild-Type Strain CN1020 and Its Genetically Modified Derivatives.$h[electronic resource] 260 $c2015 520 $aAbstract Clostridium perfringens type D causes enterotoxemia in sheep and goats. The disease is mediated by epsilon toxin (ETX), which affects the cerebrovascular endothelium, increasing vascular permeability and leading to cerebral edema. In the present study, we compared the distribution and severity of the cerebrovascular changes induced in lambs by C. perfringens type D strain CN1020, its isogenic etx null mutant, and the ETX-producing complemented mutant. We also applied histochemical and immunohistochemical markers to further characterize the brain lesions induced by ETX. Both ETX-producing strains induced extensive cerebrovascular damage that did not differ significantly between each other in nature, neuroanatomic distribution, or severity. By contrast, lambs inoculated with the etx mutant or sterile, nontoxic culture medium did not develop detectable brain lesions, confirming that the neuropathologic effects observed in these infections are dependent on ETX production. Lambs treated with the wild-type and complemented strains showed perivascular and mural vascular edema, as well as serum albumin extravasation, particularly severe in the cerebral white matter, midbrain, medulla oblongata, and cerebellum. Brains of animals inoculated with the ETX-producing strains showed decreased expression of glial fibrillary acidic protein and increased expression of aquaporin-4 in the end-feet processes of the astrocytes around blood vessels. Early axonal injury was demonstrated with anti?amyloid precursor protein immunohistochemistry. Perivascular accumulation of macrophages/microglia with intracytoplasmic albumin globules was also observed in these animals. This study demonstrates that ETX is responsible for the major cerebrovascular changes in C. perfringens type D?induced disease. 650 $aENFERMEDADES DE LOS ANIMALES 700 1 $aGIANNITTI, F. 700 1 $aFINNIE, J.W. 700 1 $aMANAVIS, J. . 700 1 $aBEINGESSER, J. 700 1 $aADAMS ,V. 700 1 $aROOD, J.I. 700 1 $aUZAL, F.A. 773 $tVeterinary Pathology, 2015$gv.52.n.6. p.1250-1253, 2015.
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Biblioteca (s) : |
INIA La Estanzuela. |
Fecha actual : |
03/01/2019 |
Actualizado : |
07/06/2019 |
Tipo de producción científica : |
Artículos en Revistas Indexadas Internacionales |
Circulación / Nivel : |
Internacional - -- |
Autor : |
LEWIS ,C.M.; PERSOONS, A.; BEBBER, D.P.; KIGATHI, R.N.; MAINTZ, J.; FINDLAY, K.; BUENO-SANCHO, V.; CORREDOR-MORENO, P.; HARRINGTON, S.A.; KANGARA, N.; BERLIN, A.; GARCIA, R.; GERMAN, S.; HANZALOVÁ, A.; HODSON, D.P.; HOVMØLLER, M.S.; HUERTA-ESPINO, J.; IMTIAZ, M.; MIRZA, J.I.; JUSTESEN, A.F.; NIKS, R.E.; OMRANI, A.; PATPOUR, M.; PRETORIUS ,Z.A.; ROOHPARVAR, R.; SELA, H.; SINGH, R.P.; STEFFENSON ,B.; VISSER, B.; FENWICK, P.M.; THOMAS, J.; WULFF, B.B.H.; SAUNDERS, D.G.O. |
Afiliación : |
John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; University of Exeter, Exeter, EX4 4QD UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; ohn Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; Department of Forest Mycology and Plant Pathology, Swedish University of Agricultural Sciences, Uppsala, 750 07 Sweden; RICHARD ANSELMO GARCIA USUCA, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; SILVIA ELISA GERMAN FAEDO, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; Crop Research Institute, Ruzyn?, 161 06 Praha 6 Czech Republic.; International Maize and Wheat Improvement Center (CIMMYT), 5689 Addis Ababa, Ethiopia.; Aarhus University, Flakkebjerg, 4200 Denmark.; Campo Experimental Valle de México INIFAP, Texcoco, C. P. 56237 Mexico.; CIMMYT-Pakistan, Islamabad, 44000 Pakistan.; Crop Disease Research Program, National Agriculture Research Center, Islamabad, 44000 Pakistan.; Aarhus University, Flakkebjerg, 4200 Denmark.; Wageningen University, Wageningen, 6700 The Netherlands; Faculty of Agriculture, Department of Plant Breeding and Biotechnology, University of Tabriz, Tabriz, 5166616471 Iran.; Aarhus University, Flakkebjerg, 4200 Denmark.; University of the Free State, Bloemfontein, 9301 South Africa.; Seed and Plant Improvement Institute, Agricultural Research, Education and Extension Organization (AREEO), 4119 Karaj, Iran.; Tel Aviv University, Tel Aviv, 69978 Israel.; CIMMYT, Apdo. Postal 6-641, D. F. México, 06600 Mexico.; University of Minnesota, St. Paul, 55455 MN USA.; University of the Free State, Bloemfontein, 9301 South Africa.; Limagrain UK Ltd, Woolpit, IP30 9UP UK.; National Institute of Agricultural Botany, Cambridge, CB3 0LE UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK.; John Innes Centre, Norwich Research Park, Norwich, NR4 7UH UK. |
Título : |
Potential for re-emergence of wheat stem rust in the United Kingdom. |
Fecha de publicación : |
2018 |
Fuente / Imprenta : |
Veterinary Pathology [Vet Pathol], 2018 Sep 24, p. 300985818798117.OPEN ACCESS. |
DOI : |
10.1038/s42003-018-0013-y |
Idioma : |
Inglés |
Notas : |
Article history: Date Created: 20181002 //Latest Revision: 20181003. |
Contenido : |
Wheat stem rust, a devastating disease of wheat and barley caused by the fungal pathogen
Puccinia graminis f. sp. tritici, was largely eradicated in Western Europe during the mid-to-late
twentieth century. However, isolated outbreaks have occurred in recent years. Here we
investigate whether a lack of resistance in modern European varieties, increased presence of its
alternate host barberry and changes in climatic conditions could be facilitating its resurgence.
We report the first wheat stem rust occurrence in the United Kingdom in nearly 60 years,
with only 20% of UK wheat varieties resistant to this strain. Climate changes over the past 25
years also suggest increasingly conducive conditions for infection. Furthermore, we document
the first occurrence in decades of P. graminis on barberry in the UK . Our data illustrate that
wheat stem rust does occur in the UK and, when climatic conditions are conducive, could
severely harm wheat and barley production. |
Thesagro : |
TRIGO. |
Asunto categoría : |
-- |
URL : |
http://www.ainfo.inia.uy/digital/bitstream/item/12241/1/Commun-Biol.-2018.pdf
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Marc : |
LEADER 02459naa a2200541 a 4500 001 1059410 005 2019-06-07 008 2018 bl uuuu u00u1 u #d 024 7 $a10.1038/s42003-018-0013-y$2DOI 100 1 $aLEWIS ,C.M. 245 $aPotential for re-emergence of wheat stem rust in the United Kingdom.$h[electronic resource] 260 $c2018 500 $aArticle history: Date Created: 20181002 //Latest Revision: 20181003. 520 $aWheat stem rust, a devastating disease of wheat and barley caused by the fungal pathogen Puccinia graminis f. sp. tritici, was largely eradicated in Western Europe during the mid-to-late twentieth century. However, isolated outbreaks have occurred in recent years. Here we investigate whether a lack of resistance in modern European varieties, increased presence of its alternate host barberry and changes in climatic conditions could be facilitating its resurgence. We report the first wheat stem rust occurrence in the United Kingdom in nearly 60 years, with only 20% of UK wheat varieties resistant to this strain. Climate changes over the past 25 years also suggest increasingly conducive conditions for infection. Furthermore, we document the first occurrence in decades of P. graminis on barberry in the UK . Our data illustrate that wheat stem rust does occur in the UK and, when climatic conditions are conducive, could severely harm wheat and barley production. 650 $aTRIGO 700 1 $aPERSOONS, A. 700 1 $aBEBBER, D.P. 700 1 $aKIGATHI, R.N. 700 1 $aMAINTZ, J. 700 1 $aFINDLAY, K. 700 1 $aBUENO-SANCHO, V. 700 1 $aCORREDOR-MORENO, P. 700 1 $aHARRINGTON, S.A. 700 1 $aKANGARA, N. 700 1 $aBERLIN, A. 700 1 $aGARCIA, R. 700 1 $aGERMAN, S. 700 1 $aHANZALOVÁ, A. 700 1 $aHODSON, D.P. 700 1 $aHOVMØLLER, M.S. 700 1 $aHUERTA-ESPINO, J. 700 1 $aIMTIAZ, M. 700 1 $aMIRZA, J.I. 700 1 $aJUSTESEN, A.F. 700 1 $aNIKS, R.E. 700 1 $aOMRANI, A. 700 1 $aPATPOUR, M. 700 1 $aPRETORIUS ,Z.A. 700 1 $aROOHPARVAR, R. 700 1 $aSELA, H. 700 1 $aSINGH, R.P. 700 1 $aSTEFFENSON ,B. 700 1 $aVISSER, B. 700 1 $aFENWICK, P.M. 700 1 $aTHOMAS, J. 700 1 $aWULFF, B.B.H. 700 1 $aSAUNDERS, D.G.O. 773 $tVeterinary Pathology [Vet Pathol], 2018 Sep 24, p. 300985818798117.OPEN ACCESS.
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