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Registro completo
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Biblioteca (s) : |
INIA La Estanzuela. |
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Fecha : |
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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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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INIA La Estanzuela (LE) |
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Registro completo
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Biblioteca (s) : |
INIA Las Brujas. |
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Fecha actual : |
07/06/2022 |
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Actualizado : |
30/11/2022 |
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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 : |
MACHADO, M.; CASTRO, M.B.; WILSON, T. M.; GONÇALVES , A. A. B.; PORTIANSKY, E.; RIET-CORREA, F.; BARROS, S. S. |
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Afiliación : |
MIZAEL MACHADO DA COSTA, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; MÁRCIO B. CASTRO, University of Brasilia, Brasília, Brazil; TAIS M. WILSON, University of Brasilia, Brasília, Brazil; ALEXANDRA A. B. GONÇALVES, University of Brasilia, Brasília, Brazil; ENRIQUE L. PORTIANSKY, National University of La Plata, La Plata, Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Argentina; FRANKLIN RIET-CORREA AMARAL, INIA (Instituto Nacional de Investigación Agropecuaria), Uruguay; Federal University of Bahia, Salvador, Brazil; SEVERO S. BARROS, Federal University of Santa Maria, Rio Grande do Sul, Brazil. |
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Título : |
Poisoning by Nierembergia veitchii: Effects on vascular smooth muscle cells in the pathogenesis of enzootic calcinosis. |
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Fecha de publicación : |
2022 |
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Fuente / Imprenta : |
Veterinary Pathology, 2022, Volume 59, Issue 5, pages 814-823. doi: https://doi.org/10.1177/03009858221098430 |
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ISSN : |
0300-9858 |
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DOI : |
10.1177/03009858221098430 |
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Idioma : |
Inglés |
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Notas : |
Article history: Article first published online May 19, 2022; Published online September 2022. -- Corresponding Author: Franklin Riet-Correa, Postgraduate Program in Animal Science in the Tropics, School of Veterinary Medicine and Animal Science, Federal University of Bahia, Salvador, Bahia 40170-110, Brazil. Email: franklinrietcorrea@gmail.com -- This work was funded by National Institute of Agricultural Research (INIA) of Uruguay (Project CL 44), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Brazil, (Finance Code 001) and National University of La Plata (Project V270). A postgraduate scholarship was provided to Mizael Machado by INIA, Uruguay. |
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Contenido : |
ABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It is proposed that the two different VSMC-S phenotypes in calcinosis are due to the expression of at least two genetically different types of these cells induced by the action of 1,25(OH)2D3. © The Author(s) 2022. MenosABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It ... Presentar Todo |
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Palabras claves : |
Arterial mineralization; Arteries; Enzootic calcinosis; Exosomes; Pathogenesis; PLATAFORMA DE SALUD ANIMAL; Toxicity; Vascular smooth muscle cells. |
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Asunto categoría : |
L50 Fisiología y bioquímica animal |
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Marc : |
LEADER 03391nam a2200313 a 4500
001 1063233
005 2022-11-30
008 2022 bl uuuu u01u1 u #d
022 $a0300-9858
024 7 $a10.1177/03009858221098430$2DOI
100 1 $aMACHADO, M.
245 $aPoisoning by Nierembergia veitchii$bEffects on vascular smooth muscle cells in the pathogenesis of enzootic calcinosis.$h[electronic resource]
260 $aVeterinary Pathology, 2022, Volume 59, Issue 5, pages 814-823. doi: https://doi.org/10.1177/03009858221098430$c1177
500 $aArticle history: Article first published online May 19, 2022; Published online September 2022. -- Corresponding Author: Franklin Riet-Correa, Postgraduate Program in Animal Science in the Tropics, School of Veterinary Medicine and Animal Science, Federal University of Bahia, Salvador, Bahia 40170-110, Brazil. Email: franklinrietcorrea@gmail.com -- This work was funded by National Institute of Agricultural Research (INIA) of Uruguay (Project CL 44), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, Brazil, (Finance Code 001) and National University of La Plata (Project V270). A postgraduate scholarship was provided to Mizael Machado by INIA, Uruguay.
520 $aABSTRACT - Vascular mineralization is a hallmark of enzootic calcinosis. Histopathological, ultrastructural, and immunohistochemical investigations were performed on the external carotid arteries of seven sheep naturally poisoned by Nierembergia veitchii. Histologically, moderate to marked hyperplasia of the tunica intima was observed without mineralization. The tunica media exhibited mild to severe mineralization and osteochondroid metaplasia. Sheep with enzootic calcinosis showed arterial overexpression of osteopontin and tissue-nonspecific alkaline phosphatase and immunolabeling for osteonectin and osteocalcin in both intima and media layers of the tested arteries. The main ultrastructural finding in the tunica media was a marked phenotypic change of vascular smooth muscle cells from a contractile phenotype (VSMC-C) into a synthetic phenotype (VSMC-S). In the tunica media, VSMC-S produced matrix and extracellular vesicles, forming mineralizable granules associated with arterial mineralization. VSMC-S were also present in the tunica intima, but matrix and extracellular vesicles and mineralization were not observed. The absence of matrix and extracellular vesicles in the intimal hyperplasia, even in the presence of noncollagenous bone proteins, tissue-nonspecific alkaline phosphatase, and vitamin D receptors, reinforces the hypothesis that the presence of matrix and extracellular vesicles are crucial for the development of vascular mineralization in enzootic calcinosis. It is proposed that the two different VSMC-S phenotypes in calcinosis are due to the expression of at least two genetically different types of these cells induced by the action of 1,25(OH)2D3. © The Author(s) 2022.
653 $aArterial mineralization
653 $aArteries
653 $aEnzootic calcinosis
653 $aExosomes
653 $aPathogenesis
653 $aPLATAFORMA DE SALUD ANIMAL
653 $aToxicity
653 $aVascular smooth muscle cells
700 1 $aCASTRO, M.B.
700 1 $aWILSON, T. M.
700 1 $aGONÇALVES , A. A. B.
700 1 $aPORTIANSKY, E.
700 1 $aRIET-CORREA, F.
700 1 $aBARROS, S. S.
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