{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T06:13:54Z","timestamp":1790489634974,"version":"4.1.0"},"reference-count":24,"publisher":"American Society for Microbiology","issue":"8","license":[{"start":{"date-parts":[[2008,8,1]],"date-time":"2008-08-01T00:00:00Z","timestamp":1217548800000},"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":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2008,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Rifaximin, a poorly absorbed rifamycin derivative, is a promising alternative for the treatment of\n                    <jats:italic>Clostridium difficile<\/jats:italic>\n                    infections. Resistance to this agent has been reported, but no commercial test for rifaximin resistance exists and the molecular basis of this resistance has not been previously studied in\n                    <jats:italic>C. difficile<\/jats:italic>\n                    . To evaluate whether the rifampin Etest would be a suitable substitute for rifaximin susceptibility testing in the clinical setting, we analyzed the in vitro rifaximin susceptibilities of 80 clinical isolates from our collection by agar dilution and compared these results to rifampin susceptibility results obtained by agar dilution and Etest. We found rifaximin susceptibility data to agree with rifampin susceptibility; the MICs of both antimicrobials for all isolates were either very low or very high. Fourteen rifaximin-resistant (MIC, \u226532 \u03bcg\/ml) unique isolates from patients at diverse locations in three countries were identified. Molecular typing analysis showed that nine (64%) of these isolates belonged to the epidemic BI\/NAP1\/027 group that is responsible for multiple outbreaks and increased disease severity in the United Kingdom, Europe, and North America. The molecular basis of rifaximin and rifampin resistance in these isolates was investigated by sequence analysis of\n                    <jats:italic>rpoB<\/jats:italic>\n                    , which encodes the \u03b2 subunit of RNA polymerase, the target of rifamycins. Resistance-associated\n                    <jats:italic>rpoB<\/jats:italic>\n                    sequence differences that resulted in specific amino acid substitutions in an otherwise conserved region of RpoB were found in all resistant isolates. Seven different RpoB amino acid substitutions were identified in the resistant isolates, which were divided into five distinct groups by restriction endonuclease analysis typing. These results suggest that the amino acid substitutions associated with rifamycin resistance were independently derived rather than disseminated from specific rifamycin-resistant clones. We propose that rifaximin resistance in\n                    <jats:italic>C. difficile<\/jats:italic>\n                    results from mutations in RpoB and that rifampin resistance predicts rifaximin resistance for this organism.\n                  <\/jats:p>","DOI":"10.1128\/aac.00342-08","type":"journal-article","created":{"date-parts":[[2008,6,16]],"date-time":"2008-06-16T20:58:17Z","timestamp":1213649897000},"page":"2813-2817","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":177,"title":["Rifampin and Rifaximin Resistance in Clinical Isolates of\n                    <i>Clostridium difficile<\/i>"],"prefix":"10.1128","volume":"52","author":[{"given":"Jennifer R.","family":"O'Connor","sequence":"first","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Minerva A.","family":"Galang","sequence":"additional","affiliation":[{"name":"Loyola University Medical Center and Loyola University Stritch School of Medicine, Maywood, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan P.","family":"Sambol","sequence":"additional","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W.","family":"Hecht","sequence":"additional","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"},{"name":"Loyola University Medical Center and Loyola University Stritch School of Medicine, Maywood, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gayatri","family":"Vedantam","sequence":"additional","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"},{"name":"Loyola University Medical Center and Loyola University Stritch School of Medicine, Maywood, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dale N.","family":"Gerding","sequence":"additional","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"},{"name":"Loyola University Medical Center and Loyola University Stritch School of Medicine, Maywood, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stuart","family":"Johnson","sequence":"additional","affiliation":[{"name":"Hines Veterans Affairs Hospital, Hines, Illinois"},{"name":"Loyola University Medical Center and Loyola University Stritch School of Medicine, Maywood, Illinois"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0022-2836(05)80360-2"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(01)00286-0"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/jcm.31.7.1870-1875.1993"},{"key":"e_1_3_2_5_2","unstructured":"Clinical and Laboratory Standards Institute 2007"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.47.7.2316-2318.2003"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0005-2787(67)90147-5"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.01623-06"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0732-8893(93)90004-Q"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.44.8.2205-2206.2000"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2836(88)90517-7"},{"key":"e_1_3_2_12_2","doi-asserted-by":"crossref","first-page":"846","DOI":"10.1086\/511870","volume":"44","year":"2007","unstructured":"Johnson, S., C. Schriever, M. Galang, C. P. Kelly, and D. N. Gerding. 2007. Interruption of recurrent Clostridium difficile-associated diarrhea episodes by serial therapy with vancomycin and rifaximin. Clin. Infect. Dis.44:846-848.","journal-title":"Clin. Infect. Dis."},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.01484-07"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa051639"},{"key":"e_1_3_2_15_2","first-page":"219","year":"2007","unstructured":"Louie, T., M. Gerson, D. Grimard, S. Johnson, A. Poirier, K. Weiss, J. Peppe, J. Donovan, and D. Davidson. 2007. Results of a phase III trial comparing tolevamer, vancomycin and metronidazole in patients with Clostridium difficile-associated diarrhea (CDAD), abstr. K-425a, p. 219. Abstr. 47th Intersci. Conf. Antimicrob. Agents Chemother., American Society for Microbiology, Washington, DC.","journal-title":"Intersci. Conf. Antimicrob. 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