{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T01:47:15Z","timestamp":1791942435123,"version":"4.3.4"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2006,2,1]],"date-time":"2006-02-01T00:00:00Z","timestamp":1138752000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:italic>Yersinia pestis<\/jats:italic>\n            , the agent of plague, is usually transmitted by fleas. To produce a transmissible infection,\n            <jats:italic>Y. pestis<\/jats:italic>\n            colonizes the flea midgut and forms a biofilm in the proventricular valve, which blocks normal blood feeding. The enteropathogen\n            <jats:italic>Yersinia pseudotuberculosis<\/jats:italic>\n            , from which\n            <jats:italic>Y. pestis<\/jats:italic>\n            recently evolved, is not transmitted by fleas. However, both\n            <jats:italic>Y. pestis<\/jats:italic>\n            and\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            form biofilms that adhere to the external mouthparts and block feeding of\n            <jats:italic>Caenorhabditis elegans<\/jats:italic>\n            nematodes, which has been proposed as a model of\n            <jats:italic>Y. pestis<\/jats:italic>\n            -flea interactions. We compared the ability of\n            <jats:italic>Y. pestis<\/jats:italic>\n            and\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            to infect the rat flea\n            <jats:italic>Xenopsylla cheopis<\/jats:italic>\n            and to produce biofilms in the flea and in vitro. Five of 18\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            strains, encompassing seven serotypes, including all three serotype O3 strains tested, were unable to stably colonize the flea midgut. The other strains persisted in the flea midgut for 4 weeks but did not increase in numbers, and none of the 18 strains colonized the proventriculus or produced a biofilm in the flea.\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            strains also varied greatly in their ability to produce biofilms in vitro, but there was no correlation between biofilm phenotype in vitro or on the surface of\n            <jats:italic>C. elegans<\/jats:italic>\n            and the ability to colonize or block fleas. Our results support a model in which a genetic change in the\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            progenitor of\n            <jats:italic>Y. pestis<\/jats:italic>\n            extended its pre-existing ex vivo biofilm-forming ability to the flea gut environment, thus enabling proventricular blockage and efficient flea-borne transmission.\n          <\/jats:p>","DOI":"10.1128\/jb.188.3.1113-1119.2006","type":"journal-article","created":{"date-parts":[[2006,1,20]],"date-time":"2006-01-20T17:27:29Z","timestamp":1137778049000},"page":"1113-1119","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":60,"title":["Serotype Differences and Lack of Biofilm Formation Characterize\n            <i>Yersinia pseudotuberculosis<\/i>\n            Infection of the\n            <i>Xenopsylla cheopis<\/i>\n            Flea Vector of\n            <i>Yersinia pestis<\/i>"],"prefix":"10.1128","volume":"188","author":[{"given":"David L.","family":"Erickson","sequence":"first","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clayton O.","family":"Jarrett","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brendan W.","family":"Wren","sequence":"additional","affiliation":[{"name":"London School of Hygiene and Tropical Medicine, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. Joseph","family":"Hinnebusch","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"14043","DOI":"10.1073\/pnas.96.24.14043","volume":"96","year":"1999","unstructured":"Achtman, M., K. Zurth, G. Morelli, G. Torrea, A. Guiyoule, and E. Carniel. 1999. Yersinia pestis, the cause of plague, is a recently emerged clone of Yersinia pseudotuberculosis. Proc. Natl. Acad. Sci. USA96:14043-14048.","journal-title":"Proc. Natl. Acad. Sci. USA"},{"key":"e_1_3_2_3_2","first-page":"774","volume":"14","year":"1915","unstructured":"Bacot, A. W. 1915. Further notes on the mechanism of the transmission of plague by fleas. J. Hyg. Plague14(Suppl. 4):774-776.","journal-title":"J. Hyg. 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