title: A hospital outbreak of Clostridium difficile disease associated with isolates carrying binary toxin genes.
abstract: BACKGROUND
  The binary toxin genes cdt and cdtB have been detected in approximately 5% of Clostridium difficile strains. Severe C. difficile disease (CDD) may be associated with strains that carry the binary toxin genes.
  
  
  METHODS
  From April 2001 through March 2002, 8 severe and 41 nonsevere cases of nosocomial CDD were studied. Severe cases of CDD were defined by the presence of >or=2 of the following criteria: (1) abdominal pain, (2) a white blood cell count of >20,000 or <1500 cells/mm(3), and (3) ileus or bowel wall thickening with ascites. Underlying disease was assessed by 2 methods: a modified Horn score and the presence of comorbid conditions. The presence of cdtA, cdtB, and the toxin A and toxin B genes was determined, and molecular subtyping was performed.
  
  
  RESULTS
  All strains were positive for the toxin A and B genes, and 65.3% of the strains carried the cdtA and cdtB genes. Strains that carried the binary toxin genes accounted for 87.5% of the cases of severe CDD and 61.0% of the nonsevere cases (P=.23). Severity of CDD was not associated with either severe underlying disease or comorbid conditions. The strains that caused severe CDD belonged to 4 protein profile groups and >or=3 restriction endonuclease analysis (REA) groups. All (i.e., 5 of 5) strains in REA group BI, compared with none (i.e., 0 of 7) of the strains in REA group J carried the binary toxin genes (P=.001). Strains that belonged to REA groups BK and BR also carried the binary toxin genes.
  
  
  CONCLUSIONS
  The binary toxin genes were present in nearly two-thirds of the C. difficile strains, and they were correlated with the REA group. Severity of CDD was not closely associated with a specific clone or underlying disease, but it may be associated with the presence of the binary toxin genes. Larger studies are needed to discern whether a true association exists and whether the binary toxin alters the pathogenicity of the C. difficile strain.
authors.affiliation: University of Pittsburgh School of Medicine, Pittsburgh, PA 15213-2582, USA. mcellistremc@msx.dept-med.pitt.edu
authors.forename: M Catherine
authors.initials: MC
authors.lastname: McEllistrem
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Carman
authors.forename: Dale N
authors.initials: DN
authors.lastname: Gerding
authors.forename: C W
authors.initials: CW
authors.lastname: Genheimer
authors.forename: L
authors.initials: L
authors.lastname: Zheng
mesh_terms: D036002:ADP Ribose Transferases / Q000235:genetics; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001426:Bacterial Proteins / Q000235:genetics; D001427:Bacterial Toxins / Q000235:genetics*; D016360:Clostridioides difficile / Q000145:classification / Q000235:genetics* / Q000302:isolation & purification; D003428:Cross Infection / Q000382:microbiology*; D004196:Disease Outbreaks; D004761:Enterocolitis, Pseudomembranous / Q000382:microbiology; D006801:Humans; D008875:Middle Aged; D000091402:Prohibitins; D012189:Retrospective Studies
chemical_list: D001426:Bacterial Proteins; D001427:Bacterial Toxins; C000717331:PHB2 protein, human; D000091402:Prohibitins; D036002:ADP Ribose Transferases; C410164:actin-specific ADP-ribosyltransferase, Clostridium