n1_4mer:GRV/n1_4mer:RV = (Global Relative Variance of OU patterns) / (Local Relative Variance of OU patterns)
n0_4mer:D = Distance between local and global OU patterns
n0_4mer:PS = Distance between 2 strands of same DNA molecule
Selected loci indicated by large D, increased GRV associated with decreased RV and moderate increase in PS
NC_017179: Clostridium difficile BI1, complete genome
NCBI: NC_017179
Host Lineage: Peptoclostridium difficile; Peptoclostridium; Peptostreptococcaceae; Clostridiales; Firmicutes; Bacteria
General Information: Clostridium difficile BI1 is a human strain isolated in the United States in 1988. 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. C. difficile infection represents one of the most common nosocomial (originating in a hospital) infections. 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. Cytotoxin B depolymerizes actin, the major protein of the cytoskeleton, and thus aids in destruction of tissues. The combined action of the toxins results in necrosis of superficial epithelium and edema (fluidic swelling) in affected areas of intestine. Proliferation of C. difficile is normally prevented by normal intestinal microflora, which is believed to inhibit attachment of the bacterium and its toxins to intestinal walls. 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.