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. 2023 Jan 4;14(1):2150452. doi: 10.1080/21505594.2022.2150452

Table 1.

Virulence factors of C. difficile.

Virulence Factor Function/Evidence References
Toxin A (tcdA) Inactivate Rho GTPases. Disrupts the cytoskeleton resulting in disruption of tight junctions and loss of intestinal barrier function. (Barth et al., 2001; Egerer et al., 2009; Gerhard et al., n.d.; Jank et al., 2007; Just et al., 1995; Madan and Petri, 2012; Oezguen et al., 2012; Papatheodorou et al., 2010; Qa’Dan et al., 2000)
Toxin B (tcdB) Inactivate Rho GTPases. Disrupts the cytoskeleton resulting in disruption of tight junctions and loss of intestinal barrier function. Huge diversity of subtypes, undergoes accelerated evolution. (Barth et al., 2001; Egerer et al., 2009; Gerhard et al., n.d.; Jank et al., 2007; Just et al., 1995; Madan and Petri, 2012; Oezguen et al., 2012; Papatheodorou et al., 2010; Qa’Dan et al., 2000; Shen et al., 2020)
C. difficile binary toxin (CDT) ADP-ribosyltransferase which causes depolymerisation of the actin cytoskeleton (leading to loss of barrier function and disruption of tight junctions) and microtubule protrusions (leading to increased C. difficile adherence). (Aktories et al., 2011; Gerding et al., 2014; Hemmasi et al., 2015; Papatheodorou et al., 2010; Schwan et al., 2009)
SlpA Major S-layer constituent. S-layer null strain avirulent in hamster model, and more susceptible to lysozyme and immune effectors. Mutants making more porous S-layer display increased lysozyme sensitivity. (Calabi et al., 2002; Kirk et al., 2017; Lanzoni-Mangutchi et al., 2022; Merrigan et al., 2013)
Cwp2 Implicated in adhesion. Dominant antigen in patient sera. (Bradshaw et al., 2017)
Cwp84 Required for normal S-layer production. Dominant antigen in patient sera. However, mutants fully virulent in hamster models. (Wright et al., n.d.; Kirby et al., 2009)
Cwp66 Implicated in adhesion and stress tolerance. (Waligora et al., 2001; Zhou et al., 2022)
Cwp19 Transglycosylase involved in autolysis, resulting in toxin release. (Wydau-Dematteis et al., 2018)
Cwp22 Peptidoglycan cross-linking enzyme (L,D-transpeptidase). Supports cell wall integrity. Mutation reduced toxin production, increased cell permeability and autolysis, and reduced adherence. (Peltier et al., 2011; Zhu et al., 2019)
CwpV Large phase-variable CWP. Displays auto-aggregative properties. Putatively involved in colonisation and biofilm in vivo. Confers resistance to some bacteriophage. (Lawley et al., 2009; Reynolds et al., 2011; Sekulovic et al., 2015)
CD2831 Collagen binding protein involved in adhesion, biofilm formation and immune evasion. (Arato et al., 2019)
CpbA Involved in adherence through enhancing collagen interaction and extracellular matrix adherence. (Tulli et al., 2013)
Broader virulence traits
Lysozyme resistance Resistance to hydrolysis via lysozyme due to σV activation of PgdA and PdaV. S-layer provides barrier protection. Required for successful pathogenesis in hamster models. (Callewaert and Michiels, 2010; Fagan et al., 2009; Ho et al., 2014; Kaus et al., 2020; Lanzoni-Mangutchi et al., 2022)
Biofilm Contributes to antimicrobial resistance, resistance to oxygen stress, persistence and recurrence of CDI. (Bordeleau et al., 2014; Ðapa et al., 2012; Dawson et al., 2012; Frost et al., 2021; Poquet et al., 2018; Semenyuk et al., 2015; Soavelomandroso et al., 2017)
Spore formation Essential for transmission of C. difficile and resistance to environmental stressors, such as oxygen, heat and UV damage. Enables disease persistence. Increased sporulation efficiency possibly increases disease transmission. (Burns et al., 2011; Donnelly et al., 2016; Fimlaid et al., 2013; Merrigan et al., 2013; Nerber and Sorg, 2021; Setlow, 2007, 2006)
tcdC truncation Truncation thought to increase production of toxins A and B, associated with hypervirulence in ribotype 027 strains. (Carter et al., 2011; Gerding et al., 2014; Warny et al., 2005)