NC_009089:3142976 Clostridium difficile 630, complete genome
Host Lineage: Peptoclostridium difficile; Peptoclostridium; Peptostreptococcaceae; Clostridiales; Firmicutes; Bacteria
General Information: This strain is the epidemic type X variant that has been extensively studied in research and clinical laboratories. It produces both toxin A, and B. Causative agent of pseudomembranous colitis. This genus comprises about 150 metabolically diverse species of anaerobes that are ubiquitous in virtually all anoxic habitats where organic compounds are present, including soils, aquatic sediments and the intestinal tracts of animals and humans. This shape is attributed to the presence of endospores that develop under conditions unfavorable for vegetative growth and distend single cells terminally or sub-terminally. Spores germinate under conditions favorable for vegetative growth, such as anaerobiosis and presence of organic substrates. It is believed that present day Mollicutes (Eubacteria) have evolved regressively (i.e., by genome reduction) from gram-positive clostridia-like ancestors with a low GC content in DNA. Some species are capable of producing organic solvents (acetone, ethanol, etc,), molecular hydrogen and other useful compounds. This species is now recognized as the major causative agent of pseudomembranous colitis (inflammation of the colon) and diarrhea that may occur following antibiotic treatment. This bacterium causes a wide spectrum of disease, ranging from mild, self-limiting diarrhea to serious diarrhea and, in some cases, complications such as pseudomembrane formation, toxic megacolon (dilation of the colon) and peritonitis, which often lead to lethality among patients. The bacteria produce high molecular mass polypeptide cytotoxins, A and B. Some strains produce only one of the toxins, others produce both. Toxin A causes inflammatory reaction involving hypersecretion of fluid and hemorrhagic necrosis through triggering cytokine release by neutrophils. Alteration of intestinal microbial balance with antibiotic therapy and increased exposure to the bacterium in a hospital setting allows C. difficile to colonize susceptible individuals. Moreover, it has been shown that subinhibitory concentrations of antibiotics promote increased toxin production by C. difficile.