Abstract
BackgroundClostridium 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.ResultsPhylogenetic 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.ConclusionsGenome 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-1613-2) contains supplementary material, which is available to authorized users.
Highlights
Clostridium sordellii can cause severe infections in animals and humans, the latter associated with trauma, toxic shock and often-fatal gynaecological infections
Correlation of TcsL production and disease suggests that TcsL is required for C. sordellii to induce toxic shock syndrome [10]; while the tcsL+/ tcsH − strain ATCC9714 is rapidly lethal in a mouse model of infection, mutation of tcsL results in a complete loss of virulence [13]
The majority of C. sordellii strains do not encode the Large Clostridial Cytotoxins TcsL and TcsH When analysing the initial sequence assemblies we noticed that few strains appeared to contain the genes encoding the LCCs TcsL and TcsH
Summary
Clostridium sordellii can cause severe infections in animals and humans, the latter associated with trauma, toxic shock and often-fatal gynaecological infections. Clostridium sordellii is an anaerobic, Gram-positive, spore-forming species of bacterium [1] It is commonly found in the soil, and can be found in the gut of animals, including humans [2]; it has been identified in the vaginal microbiota of a small percentage of women [3]. Human C. sordellii infections are rare but can cause a variety of serious diseases, including myonecrosis and toxic shock syndrome [4,5,6]. Correlation of TcsL production and disease suggests that TcsL is required for C. sordellii to induce toxic shock syndrome [10]; while the tcsL+/ tcsH − strain ATCC9714 is rapidly lethal in a mouse model of infection, mutation of tcsL results in a complete loss of virulence [13]. Certain strains of C. sordellii lacking LCCs have been associated with less severe infections in humans [14, 15]
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