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Article

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

1
US Army Medical Research Institute for Infectious Diseases, 1425 Porter St., Fort Detrick, MD 21702, USA
2
Bacterial Respiratory and Medical Countermeasures Branch, US Food and Drug Administration, 10903 New Hampshire Avenue, Silver Spring, MD 20993, USA
3
Joint Program Management Office, Medical Countermeasure Systems, 1564 Freedman Drive, Fort Detrick, MD 21702, USA
4
University of Nebraska Medical Center, College of Public Health, 42nd and Emile, Omaha, NE 68198, USA
*
Author to whom correspondence should be addressed.
Viruses 2018, 10(10), 513; https://doi.org/10.3390/v10100513
Received: 29 July 2018 / Revised: 16 September 2018 / Accepted: 18 September 2018 / Published: 20 September 2018
(This article belongs to the Collection Advances in Ebolavirus, Marburgvirus, and Cuevavirus Research)
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. View Full-Text
Keywords: Ebola virus; intestinal tract; rhesus macaque; Macaca mulatta; kikwit; necrosis; hemorrhage; bacterial translocation; antibiotics Ebola virus; intestinal tract; rhesus macaque; Macaca mulatta; kikwit; necrosis; hemorrhage; bacterial translocation; antibiotics
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MDPI and ACS Style

Reisler, R.B.; Zeng, X.; Schellhase, C.W.; Bearss, J.J.; Warren, T.K.; Trefry, J.C.; Christopher, G.W.; Kortepeter, M.G.; Bavari, S.; Cardile, A.P. Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates. Viruses 2018, 10, 513. https://doi.org/10.3390/v10100513

AMA Style

Reisler RB, Zeng X, Schellhase CW, Bearss JJ, Warren TK, Trefry JC, Christopher GW, Kortepeter MG, Bavari S, Cardile AP. Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates. Viruses. 2018; 10(10):513. https://doi.org/10.3390/v10100513

Chicago/Turabian Style

Reisler, Ronald B., Xiankun Zeng, Christopher W. Schellhase, Jeremy J. Bearss, Travis K. Warren, John C. Trefry, George W. Christopher, Mark G. Kortepeter, Sina Bavari, and Anthony P. Cardile. 2018. "Ebola Virus Causes Intestinal Tract Architectural Disruption and Bacterial Invasion in Non-Human Primates" Viruses 10, no. 10: 513. https://doi.org/10.3390/v10100513

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