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Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus

Most species of the genus Elizabethkingia are pathogenic to humans and animals, most commonly causing meningitis. However, our understanding of the pathogenic mechanisms involved is poor and there have been few pathological studies of Elizabethkingia spp. in animals. To understand the host injury in...

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Autores principales: Huang, Xiaoli, Feng, Yang, Tang, Hong, Xiong, Guanqing, Li, Liangyu, Yang, Yucen, Wang, Kaiyu, Ouyang, Ping, Geng, Yi, Chen, Defang, Yang, Shiyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6766677/
https://www.ncbi.nlm.nih.gov/pubmed/31641424
http://dx.doi.org/10.1155/2019/6407524
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author Huang, Xiaoli
Feng, Yang
Tang, Hong
Xiong, Guanqing
Li, Liangyu
Yang, Yucen
Wang, Kaiyu
Ouyang, Ping
Geng, Yi
Chen, Defang
Yang, Shiyong
author_facet Huang, Xiaoli
Feng, Yang
Tang, Hong
Xiong, Guanqing
Li, Liangyu
Yang, Yucen
Wang, Kaiyu
Ouyang, Ping
Geng, Yi
Chen, Defang
Yang, Shiyong
author_sort Huang, Xiaoli
collection PubMed
description Most species of the genus Elizabethkingia are pathogenic to humans and animals, most commonly causing meningitis. However, our understanding of the pathogenic mechanisms involved is poor and there have been few pathological studies of Elizabethkingia spp. in animals. To understand the host injury induced by Elizabethkingia spp., we established a model of E. miricola infection in the black-spotted frog (Pelophylax nigromaculatus). The systematic pathology in and oxidative damage in the infection model were investigated. Our results show that recently isolated E. miricola is a bacterium that mainly parasitizes the host brain and that neurogenic organs are the predominant sites of damage. Infection mainly manifested as severe brain abscesses, meningoencephalitis, necrotic spondylitis, and necrotic retinitis. The liver, spleen, kidney, gastrointestinal tract, and lung were also affected to varying degrees, with bacterial necrotic inflammation. P. nigromaculatus also suffered enormous damage to its oxidative system during E. miricola infection, which may have further aggravated its disease state. Our results provide a preliminary reference for the study and treatment of Elizabethkingia spp.-induced neurological diseases in animals.
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spelling pubmed-67666772019-10-22 Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus Huang, Xiaoli Feng, Yang Tang, Hong Xiong, Guanqing Li, Liangyu Yang, Yucen Wang, Kaiyu Ouyang, Ping Geng, Yi Chen, Defang Yang, Shiyong Oxid Med Cell Longev Research Article Most species of the genus Elizabethkingia are pathogenic to humans and animals, most commonly causing meningitis. However, our understanding of the pathogenic mechanisms involved is poor and there have been few pathological studies of Elizabethkingia spp. in animals. To understand the host injury induced by Elizabethkingia spp., we established a model of E. miricola infection in the black-spotted frog (Pelophylax nigromaculatus). The systematic pathology in and oxidative damage in the infection model were investigated. Our results show that recently isolated E. miricola is a bacterium that mainly parasitizes the host brain and that neurogenic organs are the predominant sites of damage. Infection mainly manifested as severe brain abscesses, meningoencephalitis, necrotic spondylitis, and necrotic retinitis. The liver, spleen, kidney, gastrointestinal tract, and lung were also affected to varying degrees, with bacterial necrotic inflammation. P. nigromaculatus also suffered enormous damage to its oxidative system during E. miricola infection, which may have further aggravated its disease state. Our results provide a preliminary reference for the study and treatment of Elizabethkingia spp.-induced neurological diseases in animals. Hindawi 2019-09-18 /pmc/articles/PMC6766677/ /pubmed/31641424 http://dx.doi.org/10.1155/2019/6407524 Text en Copyright © 2019 Xiaoli Huang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Huang, Xiaoli
Feng, Yang
Tang, Hong
Xiong, Guanqing
Li, Liangyu
Yang, Yucen
Wang, Kaiyu
Ouyang, Ping
Geng, Yi
Chen, Defang
Yang, Shiyong
Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title_full Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title_fullStr Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title_full_unstemmed Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title_short Candidate Animal Disease Model of Elizabethkingia Spp. Infection in Humans, Based on the Systematic Pathology and Oxidative Damage Caused by E. miricola in Pelophylax nigromaculatus
title_sort candidate animal disease model of elizabethkingia spp. infection in humans, based on the systematic pathology and oxidative damage caused by e. miricola in pelophylax nigromaculatus
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6766677/
https://www.ncbi.nlm.nih.gov/pubmed/31641424
http://dx.doi.org/10.1155/2019/6407524
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