Abstract
BackgroundProteolytic Clostridium botulinum is the causative agent of botulism, a severe neuroparalytic illness. Given the severity of botulism, surprisingly little is known of the population structure, biology, phylogeny or evolution of C. botulinum. The recent determination of the genome sequence of C. botulinum has allowed comparative genomic indexing using a DNA microarray.ResultsWhole genome microarray analysis revealed that 63% of the coding sequences (CDSs) present in reference strain ATCC 3502 were common to all 61 widely-representative strains of proteolytic C. botulinum and the closely related C. sporogenes tested. This indicates a relatively stable genome. There was, however, evidence for recombination and genetic exchange, in particular within the neurotoxin gene and cluster (including transfer of neurotoxin genes to C. sporogenes), and the flagellar glycosylation island (FGI). These two loci appear to have evolved independently from each other, and from the remainder of the genetic complement. A number of strains were atypical; for example, while 10 out of 14 strains that formed type A1 toxin gave almost identical profiles in whole genome, neurotoxin cluster and FGI analyses, the other four strains showed divergent properties. Furthermore, a new neurotoxin sub-type (A5) has been discovered in strains from heroin-associated wound botulism cases. For the first time, differences in glycosylation profiles of the flagella could be linked to differences in the gene content of the FGI.ConclusionProteolytic C. botulinum has a stable genome backbone containing specific regions of genetic heterogeneity. These include the neurotoxin gene cluster and the FGI, each having evolved independently of each other and the remainder of the genetic complement. Analysis of these genetic components provides a high degree of discrimination of strains of proteolytic C. botulinum, and is suitable for clinical and forensic investigations of botulism outbreaks.
Highlights
Proteolytic Clostridium botulinum is the causative agent of botulism, a severe neuroparalytic illness
We have identified important links between coding sequences (CDSs) contained within the flagellar glycosylation island (FGI) and sugars associated with post-translational modification of flagella, and discovered a new neurotoxin A subtype associated with UK wound botulism cases
The most important aspects of the biology and evolution of proteolytic C. botulinum have been highlighted by this study, in relation to the neurotoxin and its associated cluster and the FGI
Summary
Proteolytic Clostridium botulinum is the causative agent of botulism, a severe neuroparalytic illness. The species Clostridium botulinum consists of a group of four physiologically and phylogenetically distinct Grampositive obligately anaerobic bacteria that share the common feature of producing the highly potent botulinum neurotoxin [1]. C. botulinum Group I (proteolytic C. botulinum) is a mesophilic organism that is responsible for foodborne botulism, wound botulism, adult intestinal botulism and infant botulism. C. botulinum Group II (non-proteolytic C. botulinum) is a psychrotrophic organism associated with most cases of foodborne botulism not attributed to Group I [3,4]. The botulinum neurotoxins are the most potent toxins known, with as little as 30–100 ng constituting a potentially fatal dose [5], and are considered to be a bioterrorism threat [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
