Polysaccharide lyase PL3.3 possibly potentiating Clostridioides difficile clinical symptoms based on complete genome

Sen Zhang1,2, Wen Ma1,2, Xin Zhang1

  • 1Department of Clinical Laboratory, Zibo Central Hospital, 54 Gongqingtuan West Road, Zhangdian District, Zibo, Shandong, 255000, P.R. China.

Insights

Clostridioides difficile strains RT046/ST35 and RT012/ST54 were compared. The RT046/ST35 strain, linked to severe infections, showed more genomic islands and polysaccharide lyase (PL), potentially explaining its increased virulence.

Area of Science:

  • Microbiology
  • Genomics
  • Infectious Diseases

Background:

  • Clostridioides difficile is a significant cause of hospital-acquired infectious diarrhea globally.
  • Antibiotic misuse contributes to the rise of C. difficile infections.
  • Previous research indicated RT046/ST35 strains cause more severe symptoms than RT012/ST54 strains.

Purpose of the Study:

  • To compare the genomes of C. difficile RT046/ST35 and RT012/ST54 strains.
  • To identify genomic differences that may explain the varying clinical severity associated with these strains.

Main Methods:

  • Whole-genome sequencing was employed for comparative genomic analysis.
  • Bioinformatic tools were used for genome annotation (eggNOG, KEGG, GO) and identification of genomic features.
  • Plasmid detection and genomic island analysis were performed.

Main Results:

  • The RT046/ST35 strain possesses a larger genome and more genomic islands than RT012/ST54.
  • Polysaccharide lyase (PL) was identified in the RT046/ST35 strain.
  • No significant differences were found in eggNOG or KEGG annotations, but GO annotation revealed more mRNA processes in RT046/ST35.
  • The increased clinical severity was not linked to known virulence factors but potentially to PL.

Conclusions:

  • The polysaccharide lyase (PL) in the RT046/ST35 C. difficile strain is a potential key factor contributing to more severe clinical symptoms.
  • Genomic comparison highlights the importance of specific genes, like PL, in pathogen virulence.
  • Further research is warranted to elucidate the precise role of PL in C. difficile pathogenesis.