Co‐production of Tet(X) and MCR‐1, two resistance enzymes by a single plasmid. (22nd February 2021)

• Record Type: Journal Article
• Authors: Xu, Yongchang; Liu, Lizhang; Zhang, Huimin; Feng, Youjun
• Other Names: Ramirez Santiago Castillo guestEditor.; Ghaly Timothy guestEditor.; Gillings Michael guestEditor.
• Is Part Of: Environmental microbiology. Volume 23:Number 12(2021)
• Page Start: 7445
• Page End: 7464
• Publication Date: 2021-02-22
• Subjects: Microbial ecology -- Periodicals; Environmental Microbiology -- Periodicals; 579.17
• DOI: 10.1111/1462-2920.15425
• Languages: English
• ISSNs: 1462-2912

Abstract

Summary: Tigecycline and colistin are few of 'last‐resort' antibiotic defences used in anti‐infection therapies against carbapenem‐resistant bacterial pathogens. The successive emergence of plasmid‐borne tet (X) tigecycline resistance mechanism and mobile colistin resistance ( mcr ) determinant, renders them clinically useless. Here, we report that co‐carriage of tet (X6) and mcr‐1 gives co‐resistance to both classes of antibiotics by a single plasmid in Escherichia coli . Tet(X6), the new tigecycline resistance enzyme is functionally defined. Both Tet(X6) and MCR‐1 robustly interfere accumulation of antibiotic‐induced reactive oxygen species (ROS). Unlike that mcr‐1 exerts fitness cost in E . coli, tet (X6) does not. In the tet (X6)‐positive strain that co‐harbors mcr‐1, tigecycline resistance is independently of colistin resistance caused by MCR‐1‐mediated lipid A remodelling, and vice versa . In general consistency with that of MCR‐1, Tet(X6) leads to the failure of tigecycline treatment in the infection model of G . mellonella . Taken together, the co‐production of Tet(X) and MCR‐1 appears as a major clinic/public health concern.