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| Registros recuperados : 104 | |
| 64. |  | QUIROZ GARCÍA, J.; CSEH, S.; CAMPERO, C.; BARTOLOMÉ, J. Evaluación del humor acuoso y de líquido cefalorraquídeo como estimadores del nivel de magnesio, calcio y fósforo en suero de ovinos y bovinos ln: Jornadas Uruguayas de Buiatría, 25.; Congreso Latinoamericano, 9., 1997, Paysandú, Uruguay Trabajos presentados. Paysandú (Uruguay): Centro Médico Veterinario de Paysandú, 1997. P, p. 27-28| Biblioteca(s): INIA Tacuarembó; INIA Treinta y Tres. |
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| 76. | | GARCIA, J.A.; FORMOSO, F.; REBUFFO, M.; COLL, J. Variedades forrajeras I. Colonia (Uruguay): CIAAB, 1983. 39 p. (CIAAB Miscelánea; 55) En esta publicación se pretende, en primer lugar, resumir toda la información que La Estanzuela ha acumulado en sus experimentos de evaluación comparativa de cultivares forrajeros en los últimos años. En segundo lugar, y teniendo en...| Biblioteca(s): INIA La Estanzuela. |
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| 79. | | GIANNITTI, F.; MACIAS RIOSECO, M.; GARCIA, J.; BEINGESSER, J.; WOODS, L.; PUSCHNER, B.; UZAL, F. Diagnostic exercise: hemolysis and sudden death in lambs. Veterinary Pathology, 2014, v.51, n.3, p. 623-626.| Biblioteca(s): INIA La Estanzuela. |
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| 80. | | INIA LA ESTANZUELA; GARCIA, J.A.; REBUFFO, M.; FORMOSO, F.; REAL, D.; RESTAINO, E. Forrajeras y producción de semilla fina. JORNADA, NOVIEMBRE, LA ESTANZUELA, COLONIA, URUGUAY,1992. Colonia (Uruguay): INIA , 1990. 27 p.| Biblioteca(s): INIA Tacuarembó. |
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 | Acceso al texto completo restringido a Biblioteca INIA La Estanzuela. Por información adicional contacte bib_le@inia.org.uy. |
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Registro completo
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Biblioteca (s) : |
INIA La Estanzuela. |
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Fecha actual : |
29/10/2020 |
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Actualizado : |
27/01/2021 |
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Tipo de producción científica : |
Artículos en Revistas Indexadas Internacionales |
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Circulación / Nivel : |
Internacional - -- |
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Autor : |
GIANNITTI, F.; GARCÍA, J.P.; ROOD, J.I.; ADAMS, V.; ARMENDANO, J.I.; BEINGESSER, J.; UZAL, F.A. |
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Afiliación : |
FEDERICO GIANNITTI, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; JORGE P. GARCÍA, Universidad Nacional del Centro de la Provincia de Buenos Aires (UNCPBA), Tandil, Buenos Aires, Argentina.; JULIAN I. ROOD, Monash University, Clayton, Victoria, Australia.; VICKI ADAMS, Monash University, Clayton, Victoria, Australia; JOAQUÍN I. ARMENDANO, Universidad Nacional del Centro de la Provincia de Buenos Aires (UNCPBA), Tandil, Buenos Aires, Argentina.; JULIANN BEINGESSER, University of California at Davis, San Bernardino, CA, USA.; FRANCISCO A. UZAL, University of California at Davis, San Bernardino, CA, USA. |
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Título : |
Cardiopulmonary Lesions in Sheep Produced by Experimental Acute Clostridium Perfringens Type D Enterotoxemia. |
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Fecha de publicación : |
2021 |
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Fuente / Imprenta : |
Veterinay Pathology, volumen 58, number 1, pag. 103-113, 2021. Doi: https://doi.org/10.1177/0300985820965554 |
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DOI : |
10.1177/0300985820965554 |
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Idioma : |
Inglés |
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Notas : |
Article history: First Published October 15, 2020. Corresponding Author:Francisco A. Uzal, Email: fuzal@cahfs.ucdavis.edu. The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Federico Giannitti acknowledges support from the Uruguayan ?Agencia Nacional de Investigaci ´on e Innovaci ´on? (ANII) through mobility grant MOV_CA_2018_1_150021. This work was supported by Grant R01 AI056177 from the National Institute of Allergy and Infectious Diseases (NIAID). Research at Monash University was also supported by funding provided by the Australian Research Council to the Australian Research Council Centre of Excellence in Structural and Functional Microbial Genomics (Grant CE0562063). |
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Contenido : |
Abstract:Enterotoxemia caused by Clostridium perfringens type D is one of the most prevalent clostridial diseases of sheep. The lesions of
the acute form of this disease, particularly the cerebral lesions, are well characterized; however, detailed descriptions of the cardiac and pulmonary lesions are lacking. Here we describe cardiopulmonary lesions in experimental acute type D enterotoxemia in sheep and determine the role of epsilon toxin (ETX) in the development of these lesions. Four groups of 6 sheep were intraduodenally inoculated with either a wild-type C. perfringens type D strain; its etx knockout mutant, which is unable to produce ETX; the etx mutant complemented with the wild-type etx gene, which regains the ETX toxigenic ability; or sterile culture
medium as a control. All sheep were subjected to postmortem examination within 24 hours of inoculation. Lesion scores were compared between groups for pulmonary edema; hydrothorax; ascites; hydropericardium; endocardial, myocardial and epicardial hemorrhages; microscopic lesions of acute myocardial degeneration and necrosis; and myocardial, endocardial, and epicardial edema, hemorrhage, and inflammation. Only sheep inoculated with the wild-type and complemented ETX-toxigenic bacterial strains developed cardiopulmonary lesions, which were present in varying degrees of severity and proportions. These lesions were not present in sheep inoculated with the etx mutant or in the negative control. We conclude that severe acute cardiopulmonary lesions in sheep with experimental enterotoxemia are associated with the capacity of the strains to produce ETX. These changes are likely contributors to the clinical signs and even death of affected animals. MenosAbstract:Enterotoxemia caused by Clostridium perfringens type D is one of the most prevalent clostridial diseases of sheep. The lesions of
the acute form of this disease, particularly the cerebral lesions, are well characterized; however, detailed descriptions of the cardiac and pulmonary lesions are lacking. Here we describe cardiopulmonary lesions in experimental acute type D enterotoxemia in sheep and determine the role of epsilon toxin (ETX) in the development of these lesions. Four groups of 6 sheep were intraduodenally inoculated with either a wild-type C. perfringens type D strain; its etx knockout mutant, which is unable to produce ETX; the etx mutant complemented with the wild-type etx gene, which regains the ETX toxigenic ability; or sterile culture
medium as a control. All sheep were subjected to postmortem examination within 24 hours of inoculation. Lesion scores were compared between groups for pulmonary edema; hydrothorax; ascites; hydropericardium; endocardial, myocardial and epicardial hemorrhages; microscopic lesions of acute myocardial degeneration and necrosis; and myocardial, endocardial, and epicardial edema, hemorrhage, and inflammation. Only sheep inoculated with the wild-type and complemented ETX-toxigenic bacterial strains developed cardiopulmonary lesions, which were present in varying degrees of severity and proportions. These lesions were not present in sheep inoculated with the etx mutant or in the negative control. We conclude that severe acute ... Presentar Todo |
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Palabras claves : |
CLOSTRIDIUM PERFRINGENS TYPE D; EPSILON TOXIN; HEART; LUNGS; PATHOLOGY; PLATAFORMA SALUD ANIMAL; SHEEP. |
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Thesagro : |
ENFERMEDADES DE LOS ANIMALES; OVEJA. |
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Asunto categoría : |
-- |
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Marc : |
LEADER 03466naa a2200325 a 4500
001 1061439
005 2021-01-27
008 2021 bl uuuu u00u1 u #d
024 7 $a10.1177/0300985820965554$2DOI
100 1 $aGIANNITTI, F.
245 $aCardiopulmonary Lesions in Sheep Produced by Experimental Acute Clostridium Perfringens Type D Enterotoxemia.$h[electronic resource]
260 $c2021
500 $aArticle history: First Published October 15, 2020. Corresponding Author:Francisco A. Uzal, Email: fuzal@cahfs.ucdavis.edu. The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: Federico Giannitti acknowledges support from the Uruguayan ?Agencia Nacional de Investigaci ´on e Innovaci ´on? (ANII) through mobility grant MOV_CA_2018_1_150021. This work was supported by Grant R01 AI056177 from the National Institute of Allergy and Infectious Diseases (NIAID). Research at Monash University was also supported by funding provided by the Australian Research Council to the Australian Research Council Centre of Excellence in Structural and Functional Microbial Genomics (Grant CE0562063).
520 $aAbstract:Enterotoxemia caused by Clostridium perfringens type D is one of the most prevalent clostridial diseases of sheep. The lesions of the acute form of this disease, particularly the cerebral lesions, are well characterized; however, detailed descriptions of the cardiac and pulmonary lesions are lacking. Here we describe cardiopulmonary lesions in experimental acute type D enterotoxemia in sheep and determine the role of epsilon toxin (ETX) in the development of these lesions. Four groups of 6 sheep were intraduodenally inoculated with either a wild-type C. perfringens type D strain; its etx knockout mutant, which is unable to produce ETX; the etx mutant complemented with the wild-type etx gene, which regains the ETX toxigenic ability; or sterile culture medium as a control. All sheep were subjected to postmortem examination within 24 hours of inoculation. Lesion scores were compared between groups for pulmonary edema; hydrothorax; ascites; hydropericardium; endocardial, myocardial and epicardial hemorrhages; microscopic lesions of acute myocardial degeneration and necrosis; and myocardial, endocardial, and epicardial edema, hemorrhage, and inflammation. Only sheep inoculated with the wild-type and complemented ETX-toxigenic bacterial strains developed cardiopulmonary lesions, which were present in varying degrees of severity and proportions. These lesions were not present in sheep inoculated with the etx mutant or in the negative control. We conclude that severe acute cardiopulmonary lesions in sheep with experimental enterotoxemia are associated with the capacity of the strains to produce ETX. These changes are likely contributors to the clinical signs and even death of affected animals.
650 $aENFERMEDADES DE LOS ANIMALES
650 $aOVEJA
653 $aCLOSTRIDIUM PERFRINGENS TYPE D
653 $aEPSILON TOXIN
653 $aHEART
653 $aLUNGS
653 $aPATHOLOGY
653 $aPLATAFORMA SALUD ANIMAL
653 $aSHEEP
700 1 $aGARCÍA, J.P.
700 1 $aROOD, J.I.
700 1 $aADAMS, V.
700 1 $aARMENDANO, J.I.
700 1 $aBEINGESSER, J.
700 1 $aUZAL, F.A.
773 $tVeterinay Pathology, volumen 58, number 1, pag. 103-113, 2021. Doi: https://doi.org/10.1177/0300985820965554
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