A unique megaplasmid contributes to stress tolerance and pathogenicity of an emergent Salmonella enterica serovar Infantis strain. (7th January 2014)

• Record Type: Journal Article
• Authors: Aviv, Gili; Tsyba, Katherine; Steck, Natalie; Salmon‐Divon, Mali; Cornelius, Antje; Rahav, Galia; Grassl, Guntram A,; Gal‐Mor, Ohad
• Is Part Of: Environmental microbiology. Volume 16:Number 4(2014:Apr.)
• Page Start: 977
• Page End: 994
• Publication Date: 2014-01-07
• Subjects: Microbial ecology -- Periodicals; Environmental Microbiology -- Periodicals; 579.17
• DOI: 10.1111/1462-2920.12351
• Languages: English
• ISSNs: 1462-2912

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Of all known <italic>S</italic><italic>almonella enterica </italic>serovars, <italic>S</italic>. Infantis is one of the most commonly isolated and has been recently emerging worldwide. To understand the recent emergence of <italic>S</italic>. Infantis in Israel, we performed extensive comparative analyses between pre‐emergent and the clonal emergent <italic>S</italic>. Infantis populations. We demonstrate the fixation of adaptive mutations in the DNA gyrase (<italic>gyrA</italic>) and nitroreductase (<italic>nfsA</italic>) genes, conferring resistance to quinolones and nitrofurans, respectively, and the carriage of an emergent‐specific plasmid, designated pESI. This self‐transferred episome is a mosaic megaplasmid (∼280 kb), which increases bacterial tolerance to environmental mercury (<italic>mer</italic> operon) and oxidative stress, and provides further resistance to tetracycline, sulfamethoxazole and trimethoprim, most likely due to the presence of <italic>tetRA</italic>, <italic>sulI</italic> and <italic>dfrA</italic> genes respectively. Moreover, pESI carries the yersiniabactin siderophore system and two novel chaperone‐usher fimbriae. <italic>In vitro</italic> studies established that pESI conjugation into a plasmidless <italic>S</italic>. Infantis strain results in superior biofilm formation, adhesion and invasion into avian and mammalian host cells. <italic>In vivo</italic> mouse infections demonstrated higher pathogenicity and increased intestinal inflammation caused by an <italic>S</italic>. Infantis strain harboring pESI compared with the plasmidless parental strain. Our results indicate that the presence of pESI that was found only in the emergent population of <italic>S</italic>. Infantis in Israel contributes significantly to antimicrobials tolerance and pathogenicity of its carrier. It is highly likely that pESI plays a key role in the successful spread of the emergent clone that replaced the local <italic>S</italic>. Infantis community in the short time of only 2–3 years.</p> </abstract>