Abstract
Clostridioides difficile infections (CDI) have emerged over the past decade causing symptoms that range from mild, antibiotic-associated diarrhea (AAD) to life-threatening toxic megacolon. In this study, we describe a multiple and isochronal (mixed) CDI caused by the isolates DSM 27638, DSM 27639 and DSM 27640 that already initially showed different morphotypes on solid media. The three isolates belonging to the ribotypes (RT) 012 (DSM 27639) and 027 (DSM 27638 and DSM 27640) were phenotypically characterized and high quality closed genome sequences were generated. The genomes were compared with seven reference strains including three strains of the RT 027, two of the RT 017, and one of the RT 078 as well as a multi-resistant RT 012 strain. The analysis of horizontal gene transfer events revealed gene acquisition incidents that sort the strains within the time line of the spread of their RTs within Germany. We could show as well that horizontal gene transfer between the members of different RTs occurred within this multiple infection. In addition, acquisition and exchange of virulence-related features including antibiotic resistance genes were observed. Analysis of the two genomes assigned to RT 027 revealed three single nucleotide polymorphisms (SNPs) and apparently a regional genome modification within the flagellar switch that regulates the fli operon. Our findings show that (i) evolutionary events based on horizontal gene transfer occur within an ongoing CDI and contribute to the adaptation of the species by the introduction of new genes into the genomes, (ii) within a multiple infection of a single patient the exchange of genetic material was responsible for a much higher genome variation than the observed SNPs.
Highlights
Clostridioides difficile infections (CDI) have emerged over the past decade causing symptoms that range from mild, antibiotic-associated diarrhea (AAD) to life-threatening toxic megacolon
The genes encoding the toxins TcdA and TcdB assigned to the CDI virulence [16, 17] are located on the pathogenicity locus (PaLoc) which constitutes a genomic island
Phenotypic characterization Three C. difficile strains (DSM 27638, DSM 27639 and DSM 27640) exhibiting different phenotypes on solid medium have been isolated from one stool sample of a single patient suffering from CDI
Summary
Clostridioides difficile infections (CDI) have emerged over the past decade causing symptoms that range from mild, antibiotic-associated diarrhea (AAD) to life-threatening toxic megacolon. Ribotype (RT) 027 was responsible for dynamic increase of CDIs in North-America and Europe, which quadrupled the number of CDI victims between 2004 and 2007 [7] This epidemic outbreak had been successfully controlled with a decrease in CDI infection in 2008 [8, 9]. The genes encoding the toxins TcdA and TcdB assigned to the CDI virulence [16, 17] are located on the pathogenicity locus (PaLoc) which constitutes a genomic island. This indicates that HGT is involved in the evolution of toxigenic C. difficile strains [18]. Two of the strains belong to RT 027 (DSM 27638 and DSM 27640) and one to RT 012 (DSM 27639)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
