The worldwide emergence of epidemic strains of Clostridium difficile linked to increased disease severity and mortality has resulted in greater research efforts toward determining the virulence factors and pathogenesis mechanisms used by this organism to cause disease. C. difficile is an opportunist pathogen that employs many factors to infect and damage the host, often with devastating consequences. This review will focus on the role of the 2 major virulence factors, toxin A (TcdA) and toxin B (TcdB), as well as the role of other putative virulence factors, such as binary toxin, in C. difficile-mediated infection. Consideration is given to the importance of spores in both the initiation of disease and disease recurrence and also to the role that surface proteins play in host interactions.
Keywords: AAD, antibiotic associated diarrhea; C. difficile,Clostridium difficile; CDI, C. difficile infection; CDT, Clostridium difficile transferase; CDTLoc, CDT locus; CDTa, CDT enzymatic component; CDTb, CDT binding/translocation component; CST, Clostridium spiroforme toxin; CWPs, cell wall protein; Clostridium; ECF, extracytoplasmic function; HMW, high molecular weight; LMW, low molecular weight; LSR, lipolysis-stimulated lipoprotein receptor; PCR, polymerase chain reaction; PFGE, pulsed field gel electrophoresis; PaLoc, pathogenicity locus; REA, restriction endonuclease analysis; S-layer, surface layer; SLPs, S-layer proteins; TcdA, toxin A; TcdB, toxin B; antibiotic; colitis; difficile; infection; nosocomial; toxin; virulence factor; ι-toxin, iota toxin.