Skewed genomic variability in strains of the toxigenic bacterial pathogen, Clostridium perfringens

Abstract

Clostridium perfringens is a Gram-positive, anaerobic spore-forming bacterium commonly found in soil, sediments, and the human gastrointestinal tract. C. perfringens is responsible for a wide spectrum of disease, including food poisoning, gas gangrene (clostridial myonecrosis), enteritis necroticans, and non-foodborne gastrointestinal infections. The complete genome sequences of Clostridium perfringens strain ATCC 13124, a gas gangrene isolate and the species type strain, and the enterotoxin-producing food poisoning strain SM101, were determined and compared with the published C. perfringens strain 13 genome. Comparison of the three genomes revealed considerable genomic diversity with >300 unique “genomic islands” identified, with the majority of these islands unusually clustered on one replichore. PCR-based analysis indicated that the large genomic islands are widely variable across a large collection of C. perfringens strains. These islands encode genes that correlate to differences in virulence and phenotypic characteristics of these strains. Significant differences between the strains include numerous novel mobile elements and genes encoding metabolic capabilities, strain-specific extracellular polysaccharide capsule, sporulation factors, toxins, and other secreted enzymes, providing substantial insight into this medically important bacterial pathogen.

The effect of cultivar, wilting and storage period on fermentation and the clostridial community of alfalfa silage

“…It was reported that C. perfringens and C. sporogenes could ferment proteins, protein hydrolysates or amino acids and produce large amounts of acetic and butyric acids (Cato et al 1986;Allison and Macfarlane 1990;Myers et al 2006). In this study, C. perfringens and C. sporogenes have mainly contributed to the clostridial fermentation in direct-cut alfalfa silage.…”

Clostridium perfringens Type A from Broiler Chicken with Necrotic Enteritis in Kashmir Valley, India

“…This is in agreement with Lovland and Kaldhusdal (2001), who reported detection of C. perfringens in 2-6 wk broiler chickens. Furthermore, C. perfringens is auxotrophic for 13 amino acids (Myers et al, 2006) and an increase in available nutrients would thus allow C. perfringens to proliferate extensively, leading to increased intestinal toxin levels. Thus, predisposing factors are important, but it is also essential that poultry pathogenic strains should be present to induce the disease (Timbermont et al, 2011).…”

Multilocus Sequence Typing Subtypes of Poultry Clostridium perfringens Isolates Demonstrate Disease Niche Partitioning

“…Ambiguities were resolved when appropriate with the CAP3 Sequence Assembly Program (13) (http://pbil.univ-lyon1.fr/cap3.php) and by examination of the raw electropherograms in Bionumerics. Nucleotide sequence data for three Clostridium perfringens reference strains, ATCC 13124, SM101, and strain 13, were obtained from the NCBI repository and were included in subsequent analyses for purposes of comparison (24,33). Once imported, aligned, and trimmed, the sequences from all 142 isolates were compared first by allele and then by allelic profile using Bionumerics, at which point the data were used to assign each isolate to a sequence type (ST).…”

“…Such phylogenetic studies have elucidated distinct lineages associated with specific disease syndromes attributed to this pathogen. The most obvious association is a clear partitioning of strains capable of inducing food-borne illness into lineages distinct from those of strains isolated from other niches, e.g., gangrenous muscle and healthy gastrointestinal tracts (GITs) (24,28). Investigations into the genetic relationships among C. perfringens strains recovered from poultry with NE and isolates obtained from asymptomatic poultry tissues, alimentary tracts, and the production environment have identified distinct subtypes associated with NE that are capable of inducing disease in experimental NE models, whereas isolates from other lineages do not reproduce the disease (5,20,40).…”