{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T21:57:47Z","timestamp":1792706267956,"version":"4.5.0"},"reference-count":41,"publisher":"American Society for Microbiology","issue":"16","license":[{"start":{"date-parts":[[2017,8,15]],"date-time":"2017-08-15T00:00:00Z","timestamp":1502755200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R21AI095520"],"award-info":[{"award-number":["R21AI095520"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI127390"],"award-info":[{"award-number":["R01AI127390"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R25GM058905"],"award-info":[{"award-number":["R25GM058905"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Appl Environ Microbiol"],"published-print":{"date-parts":[[2017,8,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n            is the etiological agent of cholera, an acute intestinal infection in humans characterized by voluminous watery diarrhea. Cholera is spread through ingestion of contaminated food or water, primarily in developing countries that lack the proper infrastructure for proper water and sewage treatment.\n            <jats:named-content content-type=\"genus-species\">Vibrio cholerae<\/jats:named-content>\n            is an aquatic bacterium that inhabits coastal and estuarine areas, and it is known to have several environmental reservoirs, including fish. Our laboratory has recently described the use of the zebrafish as a new animal model for the study of\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            intestinal colonization, pathogenesis, and transmission. As early as 6 h after exposure to\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            , zebrafish develop diarrhea. Prior work in our laboratory has shown that this is not due to the action of cholera toxin. We hypothesize that accessory toxins produced by\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            are the cause of diarrhea in infected zebrafish. In order to assess the effects of accessory toxins in the zebrafish, it was necessary to develop a method of quantifying diarrheal volume as a measure of pathogenesis. Here, we have adapted cell density, protein, and mucin assays, along with enumeration of\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            in the zebrafish intestinal tract and in the infection water, to achieve this goal. Combined, these assays should help us determine which toxins have the greatest diarrheagenic effect in fish and, consequently, which toxins may play a role in environmental transmission.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>IMPORTANCE<\/jats:bold>\n            Identification of the accessory toxins that cause diarrhea in zebrafish can help us understand more about the role of fish in the wild as aquatic reservoirs for\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            . It is plausible that accessory toxins can act to prolong colonization and subsequent shedding of\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            back into the environment, thus perpetuating and facilitating transmission during an outbreak. It is also possible that accessory toxins help to maintain low levels of intestinal colonization in fish, giving\n            <jats:named-content content-type=\"genus-species\">V. cholerae<\/jats:named-content>\n            an advantage when environmental conditions are not optimal for survival in the water. Studies such as this one are critical because fish could be an overlooked source of cholera transmission in the environment.\n          <\/jats:p>","DOI":"10.1128\/aem.00783-17","type":"journal-article","created":{"date-parts":[[2017,6,17]],"date-time":"2017-06-17T00:30:26Z","timestamp":1497659426000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Quantifying Vibrio cholerae Enterotoxicity in a Zebrafish Infection Model"],"prefix":"10.1128","volume":"83","author":[{"given":"Kristie C.","family":"Mitchell","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology, and Biochemistry, Wayne State University School of Medicine, Detroit, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Breen","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Biochemistry, Wayne State University School of Medicine, Detroit, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Britton","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Biochemistry, Wayne State University School of Medicine, Detroit, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melody N.","family":"Neely","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Biochemistry, Wayne State University School of Medicine, Detroit, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6856-5604","authenticated-orcid":false,"given":"Jeffrey H.","family":"Withey","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Biochemistry, Wayne State University School of Medicine, Detroit, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000173"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0008607"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1673\/031.012.14901"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1207"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.8.1.48"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/292413a0"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0007352"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0705636104"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00508-07"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(00)01721-2"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.32.2.739-747.1981"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pntd.0002293"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1128\/mBio.00047-10"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.0010008"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2009.12.005"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0011558"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0510322103"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1128\/AEM.03580-13"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)15328-7"},{"key":"e_1_3_2_21_2","first-page":"G10","article-title":"Cholera toxin stimulates secretion of immunoreactive intestinal mucin","volume":"240","author":"Forstner JF","year":"1981","unstructured":"Forstner JF RoomiNWFahimREForstnerGG. 1981. 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