{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:17:33Z","timestamp":1791296253208,"version":"4.1.0"},"reference-count":15,"publisher":"Microbiology Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,11,1]]},"abstract":"<jats:p>\n                    <jats:italic>Clostridium difficile<\/jats:italic>\n                    infection (CDI) is the most common identifiable cause of diarrhoea in hospitalized patients. Current therapies rely on the administration of metronidazole or vancomycin, which reduce vegetative populations of\n                    <jats:italic>C. difficile<\/jats:italic>\n                    in the bowel. Recurrence of the disease when treatment with these antibiotics ceases indicates that metronidazole and vancomycin affect not only\n                    <jats:italic>C. difficile<\/jats:italic>\n                    but also commensal populations that normally mediate competitive exclusion. Fidaxomicin is a new antibiotic that inhibits\n                    <jats:italic>C. difficile<\/jats:italic>\n                    . Our study shows that fidaxomicin had little effect on the composition of the faecal microbiota in terms of its major phylogenetic clusters. Notably, clostridial clusters XIVa and IV, and\n                    <jats:italic>Bifidobacterium<\/jats:italic>\n                    , were much less affected by fidaxomicin compared to vancomycin treatment. These findings help to explain the substantially reduced rates of relapse following treatment of CDI with fidaxomicin in recent clinical trials.\n                  <\/jats:p>","DOI":"10.1099\/mic.0.042010-0","type":"journal-article","created":{"date-parts":[[2010,8,19]],"date-time":"2010-08-19T21:00:37Z","timestamp":1282251637000},"page":"3354-3359","source":"Crossref","is-referenced-by-count":188,"title":["A new macrocyclic antibiotic, fidaxomicin (OPT-80), causes less alteration to the bowel microbiota of Clostridium difficile-infected patients than does vancomycin"],"prefix":"10.1099","volume":"156","author":[{"given":"Gerald W.","family":"Tannock","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Munro","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Corinda","family":"Taylor","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blair","family":"Lawley","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wayne","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brendan","family":"Byrne","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Infectious Diseases, University of Calgary, Calgary, 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