Clostridium sordellii genome analysis reveals plasmid localized toxin genes encoded within pathogenicity loci
AuthorCouchman, Edward C.
Browne, Hilary P.
Lawley, Trevor D.
Songer, J. Glenn
Fairweather, Neil F.
AffiliationDepartment of Life Sciences, Centre for Molecular Bacteriology and Infection, Imperial College London
Wellcome Trust Sanger Institute
Department of Veterinary Science and Microbiology, University of Arizona
Anaerobe Reference Laboratory, University Hospital of Wales
Veterinary Laboratories Agency
Department of Microbiology, Monash University
MetadataShow full item record
PublisherBioMed Central Ltd
CitationCouchman et al. BMC Genomics (2015) 16:392 DOI 10.1186/s12864-015-1613-2
Rights© 2015 Couchman et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0).
Collection InformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at firstname.lastname@example.org.
AbstractBACKGROUND: Clostridium sordellii can cause severe infections in animals and humans, the latter associated with trauma, toxic shock and often-fatal gynaecological infections. Strains can produce two large clostridial cytotoxins (LCCs), TcsL and TcsH, related to those produced by Clostridium difficile, Clostridium novyi and Clostridium perfringens, but the genetic basis of toxin production remains uncharacterised. RESULTS: Phylogenetic analysis of the genome sequences of 44 strains isolated from human and animal infections in the UK, US and Australia placed the species into four clades. Although all strains originated from animal or clinical disease, only 5 strains contained LCC genes: 4 strains contain tcsL alone and one strain contains tcsL and tcsH. Four toxin-positive strains were found within one clade. Where present, tcsL and tcsH were localised in a pathogenicity locus, similar to but distinct from that present in C. difficile. In contrast to C. difficile, where the LCCs are chromosomally localised, the C. sordellii tcsL and tcsH genes are localised on plasmids. Our data suggest gain and loss of entire toxigenic plasmids in addition to horizontal transfer of the pathogenicity locus. A high quality, annotated sequence of ATCC9714 reveals many putative virulence factors including neuraminidase, phospholipase C and the cholesterol-dependent cytolysin sordellilysin that are highly conserved between all strains studied. CONCLUSIONS: Genome analysis of C. sordellii reveals that the LCCs, the major virulence factors, are localised on plasmids. Many strains do not contain the LCC genes; it is probable that in several of these cases the plasmid has been lost upon laboratory subculture. Our data are consistent with LCCs being the primary virulence factors in the majority of infections, but LCC-negative strains may precipitate certain categories of infection. A high quality genome sequence reveals putative virulence factors whose role in virulence can be investigated.
VersionFinal published version
Except where otherwise noted, this item's license is described as © 2015 Couchman et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0).