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Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates

In the 2014–2016 West Africa Ebola Virus (EBOV) outbreak, there was a significant concern raised about the potential for secondary bacterial infection originating from the gastrointestinal tract, which led to the empiric treatment of many patients with antibiotics. This retrospective pathology case...

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Autores principales: Reisler, Ronald B., Zeng, Xiankun, Schellhase, Christopher W., Bearss, Jeremy J., Warren, Travis K., Trefry, John C., Christopher, George W., Kortepeter, Mark G., Bavari, Sina, Cardile, Anthony P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6213817/
https://www.ncbi.nlm.nih.gov/pubmed/30241284
http://dx.doi.org/10.3390/v10100513
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author Reisler, Ronald B.
Zeng, Xiankun
Schellhase, Christopher W.
Bearss, Jeremy J.
Warren, Travis K.
Trefry, John C.
Christopher, George W.
Kortepeter, Mark G.
Bavari, Sina
Cardile, Anthony P.
author_facet Reisler, Ronald B.
Zeng, Xiankun
Schellhase, Christopher W.
Bearss, Jeremy J.
Warren, Travis K.
Trefry, John C.
Christopher, George W.
Kortepeter, Mark G.
Bavari, Sina
Cardile, Anthony P.
author_sort Reisler, Ronald B.
collection PubMed
description In the 2014–2016 West Africa Ebola Virus (EBOV) outbreak, there was a significant concern raised about the potential for secondary bacterial infection originating from the gastrointestinal tract, which led to the empiric treatment of many patients with antibiotics. This retrospective pathology case series summarizes the gastrointestinal pathology observed in control animals in the rhesus EBOV-Kikwit intramuscular 1000 plaque forming unit infection model. All 31 Non-human primates (NHPs) exhibited lymphoid depletion of gut-associated lymphoid tissue (GALT) but the severity and the specific location of the depletion varied. Mesenteric lymphoid depletion and necrosis were present in 87% (27/31) of NHPs. There was mucosal barrier disruption of the intestinal tract with mucosal necrosis and/or ulceration most notably in the duodenum (16%), cecum (16%), and colon (29%). In the intestinal tract, hemorrhage was noted most frequently in the duodenum (52%) and colon (45%). There were focal areas of bacterial submucosal invasion in the gastrointestinal (GI) tract in 9/31 (29%) of NHPs. Only 2/31 (6%) had evidence of pancreatic necrosis. One NHP (3%) experienced jejunal intussusception which may have been directly related to EBOV. Immunofluorescence assays demonstrated EBOV antigen in CD68+ macrophage/monocytes and endothelial cells in areas of GI vascular injury or necrosis.
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spelling pubmed-62138172018-11-09 Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates Reisler, Ronald B. Zeng, Xiankun Schellhase, Christopher W. Bearss, Jeremy J. Warren, Travis K. Trefry, John C. Christopher, George W. Kortepeter, Mark G. Bavari, Sina Cardile, Anthony P. Viruses Article In the 2014–2016 West Africa Ebola Virus (EBOV) outbreak, there was a significant concern raised about the potential for secondary bacterial infection originating from the gastrointestinal tract, which led to the empiric treatment of many patients with antibiotics. This retrospective pathology case series summarizes the gastrointestinal pathology observed in control animals in the rhesus EBOV-Kikwit intramuscular 1000 plaque forming unit infection model. All 31 Non-human primates (NHPs) exhibited lymphoid depletion of gut-associated lymphoid tissue (GALT) but the severity and the specific location of the depletion varied. Mesenteric lymphoid depletion and necrosis were present in 87% (27/31) of NHPs. There was mucosal barrier disruption of the intestinal tract with mucosal necrosis and/or ulceration most notably in the duodenum (16%), cecum (16%), and colon (29%). In the intestinal tract, hemorrhage was noted most frequently in the duodenum (52%) and colon (45%). There were focal areas of bacterial submucosal invasion in the gastrointestinal (GI) tract in 9/31 (29%) of NHPs. Only 2/31 (6%) had evidence of pancreatic necrosis. One NHP (3%) experienced jejunal intussusception which may have been directly related to EBOV. Immunofluorescence assays demonstrated EBOV antigen in CD68+ macrophage/monocytes and endothelial cells in areas of GI vascular injury or necrosis. MDPI 2018-09-20 /pmc/articles/PMC6213817/ /pubmed/30241284 http://dx.doi.org/10.3390/v10100513 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Reisler, Ronald B.
Zeng, Xiankun
Schellhase, Christopher W.
Bearss, Jeremy J.
Warren, Travis K.
Trefry, John C.
Christopher, George W.
Kortepeter, Mark G.
Bavari, Sina
Cardile, Anthony P.
Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title_full Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title_fullStr Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title_full_unstemmed Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title_short Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates
title_sort ebola virus causes intestinal tract architectural disruption and bacterial invasion in non-human primates
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6213817/
https://www.ncbi.nlm.nih.gov/pubmed/30241284
http://dx.doi.org/10.3390/v10100513
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