Deciphering the role of ttrA and pduA genes for Salmonella enterica serovars in a chicken infection model

Salmonella enterica serovars use self-induced intestinal inflammation to increase electron acceptor availability and to obtain a growth advantage in the host gut. There is evidence suggesting that the ability of Salmonella to use tetrathionate and 1,2-propanediol provides an advantage in murine infe...

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Veröffentlicht in:Avian pathology 2021-05, Vol.50 (3), p.257-268
Hauptverfasser: Saraiva, M. M. S., Rodrigues Alves, L. B., Monte, D. F. M., Ferreira, T. S., Benevides, V. P., Barbosa, F. O., Freitas Neto, O. C., Almeida, A. M., Barrow, P. A., Berchieri Junior, A.
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container_end_page 268
container_issue 3
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container_title Avian pathology
container_volume 50
creator Saraiva, M. M. S.
Rodrigues Alves, L. B.
Monte, D. F. M.
Ferreira, T. S.
Benevides, V. P.
Barbosa, F. O.
Freitas Neto, O. C.
Almeida, A. M.
Barrow, P. A.
Berchieri Junior, A.
description Salmonella enterica serovars use self-induced intestinal inflammation to increase electron acceptor availability and to obtain a growth advantage in the host gut. There is evidence suggesting that the ability of Salmonella to use tetrathionate and 1,2-propanediol provides an advantage in murine infection. Thus, we present here the first study to evaluate both systemic infection and faecal excretion in commercial poultry challenged by Salmonella Enteritidis (SE) and S. Typhimurium (STM) harbouring deletions in ttrA and pduA genes, which are crucial to the metabolism of tetrathionate and 1,2-propanediol, respectively. Mutant strains were excreted at higher rates when compared to the wild-type strains. The highest rates were observed with white egg-layer and brown egg-layer chicks (67.5%), and broiler chicks (56.7%) challenged by SEΔttrAΔpduA, and brown egg-layer chicks (64.8%) challenged by STMΔttrAΔpduA. SEΔttrAΔpduA presented higher bacterial counts in the liver and spleen of the three chicken lineages and caecal contents from the broiler chickens, whereas STMΔttrAΔpduA presented higher counts in the liver and spleen of the broiler and brown-egg chickens for 28 days post-infection (P 
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M. S. ; Rodrigues Alves, L. B. ; Monte, D. F. M. ; Ferreira, T. S. ; Benevides, V. P. ; Barbosa, F. O. ; Freitas Neto, O. C. ; Almeida, A. M. ; Barrow, P. A. ; Berchieri Junior, A.</creator><creatorcontrib>Saraiva, M. M. S. ; Rodrigues Alves, L. B. ; Monte, D. F. M. ; Ferreira, T. S. ; Benevides, V. P. ; Barbosa, F. O. ; Freitas Neto, O. C. ; Almeida, A. M. ; Barrow, P. A. ; Berchieri Junior, A.</creatorcontrib><description>Salmonella enterica serovars use self-induced intestinal inflammation to increase electron acceptor availability and to obtain a growth advantage in the host gut. There is evidence suggesting that the ability of Salmonella to use tetrathionate and 1,2-propanediol provides an advantage in murine infection. Thus, we present here the first study to evaluate both systemic infection and faecal excretion in commercial poultry challenged by Salmonella Enteritidis (SE) and S. Typhimurium (STM) harbouring deletions in ttrA and pduA genes, which are crucial to the metabolism of tetrathionate and 1,2-propanediol, respectively. Mutant strains were excreted at higher rates when compared to the wild-type strains. The highest rates were observed with white egg-layer and brown egg-layer chicks (67.5%), and broiler chicks (56.7%) challenged by SEΔttrAΔpduA, and brown egg-layer chicks (64.8%) challenged by STMΔttrAΔpduA. SEΔttrAΔpduA presented higher bacterial counts in the liver and spleen of the three chicken lineages and caecal contents from the broiler chickens, whereas STMΔttrAΔpduA presented higher counts in the liver and spleen of the broiler and brown-egg chickens for 28 days post-infection (P &lt; 0.05). The ttrA and pduA genes do not appear to be major virulence determinants in faecal excretion or invasiveness for SE and STM in chickens. RESEARCH HIGHLIGHTS ttrA and pudA do not impair gut colonization or systemic infection in chicks. Mutant strains were present in higher numbers in broilers than in laying chicks. Mutants of SE and STM showed greater pathogenicity in broiler chicks than layers.</description><identifier>ISSN: 0307-9457</identifier><identifier>EISSN: 1465-3338</identifier><identifier>DOI: 10.1080/03079457.2021.1909703</identifier><identifier>PMID: 33779420</identifier><language>eng</language><publisher>England: Taylor &amp; Francis</publisher><subject>1,2-propanediol ; Chickens ; Chicks ; Colonization ; Digestive system ; Disseminated infection ; Eggs ; Excretion ; Gastrointestinal tract ; Genes ; Infections ; Invasiveness ; Juveniles ; Liver ; Metabolism ; Microbiological strains ; Mutants ; paratyphoid infection ; Pathogenicity ; Pathogens ; Poultry ; Salmonella ; Salmonella enterica ; Salmonella Enteritidis ; Salmonella Typhimurium ; salmonellosis ; Spleen ; Strains (organisms) ; Tetrathionate ; Virulence</subject><ispartof>Avian pathology, 2021-05, Vol.50 (3), p.257-268</ispartof><rights>2021 Houghton Trust Ltd 2021</rights><rights>2021 Houghton Trust Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c394t-5abff5599cc740c22940291f8f804ba20f7710bdcadd830a4c231db0194342383</citedby><cites>FETCH-LOGICAL-c394t-5abff5599cc740c22940291f8f804ba20f7710bdcadd830a4c231db0194342383</cites><orcidid>0000-0001-8021-7485 ; 0000-0002-7264-1734 ; 0000-0002-7552-1607 ; 0000-0003-3787-1988 ; 0000-0003-1178-5870 ; 0000-0003-1875-4495 ; 0000-0002-5607-0599 ; 0000-0003-2522-6500 ; 0000-0002-1437-069X ; 0000-0001-5788-5514</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33779420$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saraiva, M. M. S.</creatorcontrib><creatorcontrib>Rodrigues Alves, L. B.</creatorcontrib><creatorcontrib>Monte, D. F. M.</creatorcontrib><creatorcontrib>Ferreira, T. S.</creatorcontrib><creatorcontrib>Benevides, V. P.</creatorcontrib><creatorcontrib>Barbosa, F. O.</creatorcontrib><creatorcontrib>Freitas Neto, O. C.</creatorcontrib><creatorcontrib>Almeida, A. M.</creatorcontrib><creatorcontrib>Barrow, P. A.</creatorcontrib><creatorcontrib>Berchieri Junior, A.</creatorcontrib><title>Deciphering the role of ttrA and pduA genes for Salmonella enterica serovars in a chicken infection model</title><title>Avian pathology</title><addtitle>Avian Pathol</addtitle><description>Salmonella enterica serovars use self-induced intestinal inflammation to increase electron acceptor availability and to obtain a growth advantage in the host gut. There is evidence suggesting that the ability of Salmonella to use tetrathionate and 1,2-propanediol provides an advantage in murine infection. 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The ttrA and pduA genes do not appear to be major virulence determinants in faecal excretion or invasiveness for SE and STM in chickens. RESEARCH HIGHLIGHTS ttrA and pudA do not impair gut colonization or systemic infection in chicks. Mutant strains were present in higher numbers in broilers than in laying chicks. 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M. S.</au><au>Rodrigues Alves, L. B.</au><au>Monte, D. F. M.</au><au>Ferreira, T. S.</au><au>Benevides, V. P.</au><au>Barbosa, F. O.</au><au>Freitas Neto, O. C.</au><au>Almeida, A. M.</au><au>Barrow, P. A.</au><au>Berchieri Junior, A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deciphering the role of ttrA and pduA genes for Salmonella enterica serovars in a chicken infection model</atitle><jtitle>Avian pathology</jtitle><addtitle>Avian Pathol</addtitle><date>2021-05-04</date><risdate>2021</risdate><volume>50</volume><issue>3</issue><spage>257</spage><epage>268</epage><pages>257-268</pages><issn>0307-9457</issn><eissn>1465-3338</eissn><abstract>Salmonella enterica serovars use self-induced intestinal inflammation to increase electron acceptor availability and to obtain a growth advantage in the host gut. There is evidence suggesting that the ability of Salmonella to use tetrathionate and 1,2-propanediol provides an advantage in murine infection. Thus, we present here the first study to evaluate both systemic infection and faecal excretion in commercial poultry challenged by Salmonella Enteritidis (SE) and S. Typhimurium (STM) harbouring deletions in ttrA and pduA genes, which are crucial to the metabolism of tetrathionate and 1,2-propanediol, respectively. Mutant strains were excreted at higher rates when compared to the wild-type strains. The highest rates were observed with white egg-layer and brown egg-layer chicks (67.5%), and broiler chicks (56.7%) challenged by SEΔttrAΔpduA, and brown egg-layer chicks (64.8%) challenged by STMΔttrAΔpduA. SEΔttrAΔpduA presented higher bacterial counts in the liver and spleen of the three chicken lineages and caecal contents from the broiler chickens, whereas STMΔttrAΔpduA presented higher counts in the liver and spleen of the broiler and brown-egg chickens for 28 days post-infection (P &lt; 0.05). The ttrA and pduA genes do not appear to be major virulence determinants in faecal excretion or invasiveness for SE and STM in chickens. RESEARCH HIGHLIGHTS ttrA and pudA do not impair gut colonization or systemic infection in chicks. Mutant strains were present in higher numbers in broilers than in laying chicks. 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source Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects 1,2-propanediol
Chickens
Chicks
Colonization
Digestive system
Disseminated infection
Eggs
Excretion
Gastrointestinal tract
Genes
Infections
Invasiveness
Juveniles
Liver
Metabolism
Microbiological strains
Mutants
paratyphoid infection
Pathogenicity
Pathogens
Poultry
Salmonella
Salmonella enterica
Salmonella Enteritidis
Salmonella Typhimurium
salmonellosis
Spleen
Strains (organisms)
Tetrathionate
Virulence
title Deciphering the role of ttrA and pduA genes for Salmonella enterica serovars in a chicken infection model
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