1887

Abstract

The accessory genome of the human pathogen is large, variable and highly mobile. This reservoir of genes leads to the emergences of hospital outbreak strains with enhanced virulence and multidrug resistance, such as ST258, and acts as a source for transfer of these traits to other Gram negative pathogens. One such mobile genetic element, ICEKp, is prevalent in isolates of invasive disease where it enhances iron acquisition by the siderophore yersiniabactin. Yersiniabactin is also a virulence factor in pathogenic and species. Similarities between siderophore transporters and drug efflux pumps led us to postulate that the yersiniabactin transport proteins could contribute to antimicrobial resistance. We determined the effect of loss and gain of ICEKp, or the transporters alone, on iron acquisition and drug sensitivity of and . Deletion of ICEKp impaired iron acquisition of clinical isolate HS11286 due to reduced siderophore secretion and reduced ability to acquire iron from siderophores. A simultaneous increase in sensitivity to a broad range of antimicrobials could be complemented by reintroduction of the ybtPQ ABC transporter. Furthermore, transfer of ICEKp to occurred efficiently by conjugation and conferred a similar decrease in sensitivity to antimicrobials.

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/content/journal/acmi/10.1099/acmi.ac2020.po0414
2020-07-10
2021-02-26
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http://instance.metastore.ingenta.com/content/journal/acmi/10.1099/acmi.ac2020.po0414
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