Sze K Lim1, Rhonda L Stuart2, Kate E Mackin3, Glen P Carter3, Despina Kotsanas1, Michelle J Francis4, Marion Easton5, Karolina Dimovski5, Briony Elliott6, Thomas V Riley7, Geoff Hogg5, Eldho Paul8, Tony M Korman9, Torsten Seemann10, Timothy P Stinear11, Dena Lyras3, Grant A Jenkin12. 1. Monash Infectious Diseases, Monash Health. 2. Monash Infectious Diseases, Monash Health Department of Medicine, Southern Clinical School, Monash University. 3. Department of Microbiology, Monash University. 4. Department of Microbiology, Monash Health, Clayton. 5. Microbiological Diagnostic Unit, University of Melbourne, Parkville. 6. School of Pathology and Laboratory Medicine, The University of Western Australia. 7. School of Pathology and Laboratory Medicine, The University of Western Australia PathWest Laboratory Medicine, Nedlands. 8. School of Public Health and Preventive Medicine. 9. Monash Infectious Diseases, Monash Health Department of Medicine, Southern Clinical School, Monash University Department of Microbiology, Monash Health, Clayton. 10. Victorian Bioinformatics Consortium, Monash University, Clayton. 11. Department of Microbiology and Immunology, University of Melbourne, Parkville, Australia. 12. Monash Infectious Diseases, Monash Health Department of Microbiology, Monash University Department of Microbiology, Monash Health, Clayton Department of Microbiology and Immunology, University of Melbourne, Parkville, Australia.
Abstract
BACKGROUND: We identified 12 patients with Clostridium difficile infection between July 2011 and March 2012 from whom an unusual C. difficile strain was isolated. This strain had a single-nucleotide deletion of the tcdC gene at position 117 and binary toxin genes, which are characteristic of the hypervirulent ribotype (RT) 027 strain. METHODS: A retrospective cohort study of 12 patients infected with C. difficile RT244 and 24 patients infected with non-RT244/non-RT027 strains matched for place of diagnosis and time of collection of specimen was performed. We performed whole-genome sequencing to understand the relationship of the RT244 strain to other C. difficile strains and further understand its virulence potential. RESULTS: Clostridium difficile RT244 was associated with more severe disease and a higher mortality rate. Phylogenomic analysis using core genome single-nucleotide polymorphisms showed that RT244 is in the same genetic clade (clade 2) as RT027 but is distinct from all RT027 strains. The pathogenicity locus of the RT244 strain encodes a variant toxin B, and this was confirmed by demonstration of Clostridium sordellii-like cytopathic effect on Vero cells. Toxin B production in culture supernatants was lower than that seen with a RT027 strain. CONCLUSIONS: Our findings demonstrate the pathogenic potential of this RT244 C. difficile strain and emphasize the importance of ongoing surveillance for emergent strains.
BACKGROUND: We identified 12 patients with Clostridium difficile infection between July 2011 and March 2012 from whom an unusual C. difficile strain was isolated. This strain had a single-nucleotide deletion of the tcdC gene at position 117 and binary toxin genes, which are characteristic of the hypervirulent ribotype (RT) 027 strain. METHODS: A retrospective cohort study of 12 patients infected with C. difficile RT244 and 24 patients infected with non-RT244/non-RT027 strains matched for place of diagnosis and time of collection of specimen was performed. We performed whole-genome sequencing to understand the relationship of the RT244 strain to other C. difficile strains and further understand its virulence potential. RESULTS:Clostridium difficile RT244 was associated with more severe disease and a higher mortality rate. Phylogenomic analysis using core genome single-nucleotide polymorphisms showed that RT244 is in the same genetic clade (clade 2) as RT027 but is distinct from all RT027 strains. The pathogenicity locus of the RT244 strain encodes a variant toxin B, and this was confirmed by demonstration of Clostridium sordellii-like cytopathic effect on Vero cells. Toxin B production in culture supernatants was lower than that seen with a RT027 strain. CONCLUSIONS: Our findings demonstrate the pathogenic potential of this RT244 C. difficile strain and emphasize the importance of ongoing surveillance for emergent strains.
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