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dc.contributor.authorCharbon, Godefroid
dc.contributor.authorHaugan, Maria Schei
dc.contributor.authorFrimodt-Møller, Niels
dc.contributor.authorLøbner-Olesen, Anders
dc.date.accessioned2022-11-28T14:31:15Z
dc.date.available2022-11-28T14:31:15Z
dc.date.created2021-02-08T11:04:03Z
dc.date.issued2020
dc.identifier.citationAntibiotics 2020, 9(5), 239en_US
dc.identifier.issn2079-6382
dc.identifier.urihttps://hdl.handle.net/11250/3034565
dc.description.abstractFor the past several decades, the success of bacterial strains in infecting their host has been essentially ascribed to the presence of canonical virulence genes. While it is unclear how much growth rate impacts the outcome of an infection, it is long known that the efficacy of the most commonly used antibiotics is correlated to growth. This applies especially to β-lactams, whose efficacy is nearly abolished when cells grow very slowly. It is therefore reasonable to assume that a niche or genetic dependent change in growth rate could contribute to the variability in the outcome of antibiotic therapy. However, little is known about the growth rate of pathogens or their pathotypes in their host.en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleCounting Replication Origins to Measure Growth of Pathogensen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.volume9en_US
dc.source.journalAntibioticsen_US
dc.source.issue5en_US
dc.identifier.doi10.3390/antibiotics9050239
dc.identifier.cristin1887546
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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