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Updated: Jun 1, 2026

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Cefoperazone-treated Mouse Model of Clinically-relevant Clostridium difficile Strain R20291

Published on: December 10, 2016

Clinical Clostridium difficile: clonality and pathogenicity locus diversity.

Kate E Dingle¹, David Griffiths, Xavier Didelot

¹Nuffield Department of Clinical Laboratory Sciences, Oxford University, John Radcliffe Hospital, Oxford, United Kingdom. kate.dingle@ndcls.ox.ac.uk

|June 1, 2011

Summary

Clostridium difficile infection (CDI) strains show significant genetic diversity. Multilocus sequence typing reveals distinct clades associated with toxin variants, influencing pathogenicity and evolution of hypervirulent strains.

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Area of Science:

Microbiology
Epidemiology
Genetics

Background:

Clostridium difficile infection (CDI) is a major healthcare-associated infection.
Toxins A (tcdA) and B (tcdB) encoded by the pathogenicity locus (PaLoc) are key virulence factors.
Strain pathogenicity varies, with hypervirulent strains like PCR-ribotypes 027 and 078 causing high mortality.

Purpose of the Study:

To investigate the molecular epidemiology of Clostridium difficile.
To analyze population structure and genetic variation within toxin genes.
To understand the evolutionary origins of hypervirulent strains.

Main Methods:

Genotyping of 1290 recent CDI isolates from Oxfordshire, UK, using multilocus sequence typing (MLST).
Population structure analysis using NeighborNet and ClonalFrame.
Mapping of sequence variation in tcdB and tcdC onto the population structure.

Main Results:

69 Sequence Types (STs) were identified, with homologous recombination influencing diversification.
Five distinct genetic clades were observed, each strongly associated with specific tcdB and tcdC variants.
Hypervirulent ST-11 (078) belonged to a divergent clade (clade 5) but shared toxin gene similarity with others.

Conclusions:

MLST provides a baseline for studying CDI genotype-virulence relationships.
Genetic recombination likely plays a role in the evolution of CDI strains, including hypervirulent ones.
ST-11 (078) may have acquired the PaLoc through recombination, potentially from a previously non-toxigenic ancestor.