Nicolas Rivard received the Terry Beveridge Poster Award for his poster entitled “Antimicrobial resistance dissemination in Vibrio cholerae: mechanistic insights into the insidious role of IncC plasmids” that he presented in the Molecular Genetic & Cellular Microbiology section at CSM 2019.
Phylogenetic analysis of EexC homologues.
IncA and IncC conjugative plasmids drive the spread of antibiotic resistance among several pathogenic species of Gammaproteobacteria. While historically grouped as “IncA/C”, IncA and IncC replicons were recently confirmed to be compatible, and to abolish each other’s entry into the cell they reside in during conjugative transfer by an unknown mechanism. In a new research article published in Journal of Bacteriology, we identified an entry exclusion system (Eex) that is shared by IncA and IncC plasmids. It impedes DNA transfer to recipient cells bearing a plasmid of either incompatibility group. The entry exclusion protein of this system is unrelated to any other known entry exclusion proteins.
The 69th Annual Conference of the Canadian Society of Microbiologists (CSM 2019) will be held on the main campus of the Université de Sherbrooke in Sherbrooke, Quebec from June 10-13, 2019.
Information regarding the event can be found on the CSM2019 website.
Inter-ICE recombination plays an important role in ICE evolution
This month we published a new paper in Applied and Environmental Microbiology that reports on a comparative genomics study of a large set of unique representatives of the SXT/R391 family of integrative and conjugative elements (ICEs). These mobile elements are key players in the spread of antibiotic resistance in Vibrio cholerae and other pathogens. The SXT/R391 family of ICEs was initially defined based on the conservation of a core set of 52 genes and site-specific integration into the 5′ end of the chromosomal gene prfC. Hence, the integrase gene int has been intensively used as a marker to detect SXT/R391 ICEs in clinical and environmental isolates. With the recent reports of closely related elements that carry an alternative integrase gene, it became urgent to investigate whether ICEs that have been left out of the family are a liability for the accuracy of such screenings. Thus, we explored the prevalence and diversity of atypical ICEs in GenBank databases and their relationship with typical SXT/R391 ICEs. Our results led us to broaden the SXT/R391 family of ICEs to include atypical ICEs that are often associated with heavy metal resistance.
Alterations of the IncC mating pore by SGI1 – analysis of the working combinations
Acquisition and dissemination of multidrug resistance among Enterobacteriaceae is in part driven by IncA and IncC (A/C) conjugative plasmids, and Salmonella genomic island 1 (SGI1). Although unrelated, SGI1 relies on the self-transmissible A/C plasmids to spread within bacterial populations. How SGI1 hijacks the mating apparatus synthesized by A/C plasmids had yet to be established.
Our team published a new report in PLOS Genetics that describes yet another twist in the parasitic behavior of SGI1 towards IncC conjugative plasmids. In this report, we show that IncC plasmids trigger the expression of three SGI1-borne genes that code for functional mating pore subunits distantly related to those encoded by the IncC helper plasmids. These subunits alter the mating pore encoded by IncC plasmids to ensure optimal transfer of SGI1 and promote SGI1 dissemination in cell populations harboring IncC plasmids. Apart from SGI1 and relatives, documented mobilizable genomic islands are not known to code for mating pore components, possibly because of redundancy with those encoded by helper conjugative elements. Instead they usually code for mobilization proteins such as a relaxase and auxiliary factors involved in DNA recognition, processing and docking to the mating pore encoded by their helper conjugative element.
From an ecological and epidemiological perspective, the strategy used by SGI1 likely confers a strong competitive advantage to SGI1 over IncC plasmids in clinical settings and could account for the high prevalence of SGI1 and relatives in multidrug-resistant Salmonella enterica and Proteus mirabilis.
Vibrio cholerae, the causative agent of cholera, remains a global public health threat. Seventh-pandemic V. cholerae is known to have acquired multidrug resistance genes primarily through circulation of SXT/R391 integrative and conjugative elements. Recently, IncA/C conjugative plasmids have sporadically been reported to mediate antimicrobial resistance in environmental and clinical V. cholerae isolates. In a new paper published today in mBio, we demonstrate that while IncA/C plasmids are rare in V. cholerae populations, they play an important yet insidious role by speciﬁcally propagating a new family of genomic islands conferring resistance to multiple antibiotics. As an exemple, we report the discovery of MGIVchHai6, a genomic island found in a non-O1/non-O139 multidrug-resistant clinical isolate recovered from Haiti in 2010. MGIVchHai6 contains a mercury resistance transposon and an integron conferring resistance to β-lactams, sulfamethoxazole, tetracycline, chloramphenicol, trimethoprim, and streptomycin/spectinomycin. We present evidence that non-epidemic V. cholerae non-O1/non-O139 strains bearing similar genomic islands constitute a reservoir of transmissible resistance genes that can be propagated by IncA/C plasmids to V. cholerae populations in epidemic geographical areas as well to pathogenic species of Enterobacteriaceae.
Congratulations to Romain for his ASM student travel award!