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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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 |
doi_str_mv | 10.1080/03079457.2021.1909703 |
format | Article |
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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 & 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. 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 < 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><subject>1,2-propanediol</subject><subject>Chickens</subject><subject>Chicks</subject><subject>Colonization</subject><subject>Digestive system</subject><subject>Disseminated infection</subject><subject>Eggs</subject><subject>Excretion</subject><subject>Gastrointestinal tract</subject><subject>Genes</subject><subject>Infections</subject><subject>Invasiveness</subject><subject>Juveniles</subject><subject>Liver</subject><subject>Metabolism</subject><subject>Microbiological strains</subject><subject>Mutants</subject><subject>paratyphoid infection</subject><subject>Pathogenicity</subject><subject>Pathogens</subject><subject>Poultry</subject><subject>Salmonella</subject><subject>Salmonella enterica</subject><subject>Salmonella Enteritidis</subject><subject>Salmonella Typhimurium</subject><subject>salmonellosis</subject><subject>Spleen</subject><subject>Strains (organisms)</subject><subject>Tetrathionate</subject><subject>Virulence</subject><issn>0307-9457</issn><issn>1465-3338</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kUtvFDEQhC0EIkvgJ4AsccllNu3XzvjGKgkkUiQOwNny-JF1mLEXeyZR_j0e7YYDh5xaLX1V3apC6COBNYEOzoFBK7lo1xQoWRMJsgX2Cq0I34iGMda9RquFaRboBL0r5R4ANkLQt-iEsbaKKaxQuHQm7Hcuh3iHp53DOQ0OJ4-nKW-xjhbv7bzFdy66gn3K-IcexhTdMGjs4lR1RuPicnrQueAQscZmF8xvF-vinZlCinhM1g3v0Ruvh-I-HOcp-vX16ufFdXP7_dvNxfa2MUzyqRG6914IKY1pORhKJQcqie98B7zXFHzbEuit0dZ2DDQ3lBHbA5Gccco6dorODr77nP7MrkxqDMUsD0eX5qKoqCmAFBtW0c__ofdpzrF-VylGOeGdpJUSB8rkVEp2Xu1zGHV-UgTU0oV67kItXahjF1X36eg-96Oz_1TP4VfgywGoSaU86seUB6sm_TSk7LOOJhTFXr7xFzwmlzQ</recordid><startdate>20210504</startdate><enddate>20210504</enddate><creator>Saraiva, M. M. S.</creator><creator>Rodrigues Alves, L. B.</creator><creator>Monte, D. F. M.</creator><creator>Ferreira, T. S.</creator><creator>Benevides, V. P.</creator><creator>Barbosa, F. O.</creator><creator>Freitas Neto, O. C.</creator><creator>Almeida, A. M.</creator><creator>Barrow, P. A.</creator><creator>Berchieri Junior, A.</creator><general>Taylor & Francis</general><general>Taylor & Francis Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>7TM</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>F1W</scope><scope>H94</scope><scope>H95</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8021-7485</orcidid><orcidid>https://orcid.org/0000-0002-7264-1734</orcidid><orcidid>https://orcid.org/0000-0002-7552-1607</orcidid><orcidid>https://orcid.org/0000-0003-3787-1988</orcidid><orcidid>https://orcid.org/0000-0003-1178-5870</orcidid><orcidid>https://orcid.org/0000-0003-1875-4495</orcidid><orcidid>https://orcid.org/0000-0002-5607-0599</orcidid><orcidid>https://orcid.org/0000-0003-2522-6500</orcidid><orcidid>https://orcid.org/0000-0002-1437-069X</orcidid><orcidid>https://orcid.org/0000-0001-5788-5514</orcidid></search><sort><creationdate>20210504</creationdate><title>Deciphering the role of ttrA and pduA genes for Salmonella enterica serovars in a chicken infection model</title><author>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.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c394t-5abff5599cc740c22940291f8f804ba20f7710bdcadd830a4c231db0194342383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>1,2-propanediol</topic><topic>Chickens</topic><topic>Chicks</topic><topic>Colonization</topic><topic>Digestive system</topic><topic>Disseminated infection</topic><topic>Eggs</topic><topic>Excretion</topic><topic>Gastrointestinal tract</topic><topic>Genes</topic><topic>Infections</topic><topic>Invasiveness</topic><topic>Juveniles</topic><topic>Liver</topic><topic>Metabolism</topic><topic>Microbiological strains</topic><topic>Mutants</topic><topic>paratyphoid infection</topic><topic>Pathogenicity</topic><topic>Pathogens</topic><topic>Poultry</topic><topic>Salmonella</topic><topic>Salmonella enterica</topic><topic>Salmonella Enteritidis</topic><topic>Salmonella Typhimurium</topic><topic>salmonellosis</topic><topic>Spleen</topic><topic>Strains (organisms)</topic><topic>Tetrathionate</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><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><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Avian pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saraiva, M. 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 < 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.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>33779420</pmid><doi>10.1080/03079457.2021.1909703</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-8021-7485</orcidid><orcidid>https://orcid.org/0000-0002-7264-1734</orcidid><orcidid>https://orcid.org/0000-0002-7552-1607</orcidid><orcidid>https://orcid.org/0000-0003-3787-1988</orcidid><orcidid>https://orcid.org/0000-0003-1178-5870</orcidid><orcidid>https://orcid.org/0000-0003-1875-4495</orcidid><orcidid>https://orcid.org/0000-0002-5607-0599</orcidid><orcidid>https://orcid.org/0000-0003-2522-6500</orcidid><orcidid>https://orcid.org/0000-0002-1437-069X</orcidid><orcidid>https://orcid.org/0000-0001-5788-5514</orcidid></addata></record> |
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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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