{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T03:28:19Z","timestamp":1790911699193,"version":"4.1.0"},"reference-count":61,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2011,7,1]],"date-time":"2011-07-01T00:00:00Z","timestamp":1309478400000},"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":[[2011,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The Gram-negative bacterium\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Burkholderia pseudomallei<\/jats:named-content>\n                    is the etiological agent of melioidosis and is remarkably resistant to most classes of antibacterials. Even after months of treatment with antibacterials that are relatively effective\n                    <jats:italic>in vitro<\/jats:italic>\n                    , there is a high rate of treatment failure, indicating that this pathogen alters its patterns of antibacterial susceptibility in response to cues encountered in the host. The pathology of melioidosis indicates that\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    encounters host microenvironments that limit aerobic respiration, including the lack of oxygen found in abscesses and in the presence of nitric oxide produced by macrophages. We investigated whether\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    could survive in a nonreplicating, oxygen-deprived state and determined if this physiological state was tolerant of conventional antibacterials.\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    survived initial anaerobiosis, especially under moderately acidic conditions similar to those found in abscesses. Microarray expression profiling indicated a major shift in the physiological state of hypoxic\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    , including induction of a variety of typical anaerobic-environment-responsive genes and genes that appear specific to anaerobic\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    . Interestingly, anaerobic\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">B. pseudomallei<\/jats:named-content>\n                    was unaffected by antibacterials typically used in therapy. However, it was exquisitely sensitive to drugs used against anaerobic pathogens. After several weeks of anaerobic culture, a significant loss of viability was observed. However, a stable subpopulation that maintained complete viability for at least 1 year was established. Thus, during the course of human infection, if a minor subpopulation of bacteria inhabited an oxygen-restricted environment, it might be indifferent to traditional therapy but susceptible to antibiotics frequently used to treat anaerobic infections.\n                  <\/jats:p>","DOI":"10.1128\/aac.00953-10","type":"journal-article","created":{"date-parts":[[2011,5,2]],"date-time":"2011-05-02T22:42:03Z","timestamp":1304376123000},"page":"3313-3323","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":76,"title":["Adaptation and Antibiotic Tolerance of Anaerobic Burkholderia pseudomallei"],"prefix":"10.1128","volume":"55","author":[{"given":"Mohamad A.","family":"Hamad","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chad R.","family":"Austin","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amanda L.","family":"Stewart","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mike","family":"Higgins","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9s","family":"V\u00e1zquez-Torres","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin I.","family":"Voskuil","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Colorado School of Medicine, Aurora, Colorado 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0950268805004103"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1101\/gad.6.12b.2646"},{"key":"e_1_3_3_4_2","first-page":"85","article-title":"Innate and induced resistance mechanisms of bacterial biofilms","volume":"322","author":"Anderson G. 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