Table 1.

Enteric pathogens implicated in CRC.

Bacterium	Virulence Factors	Experimental/Epidemiological Evidence	Proposed Mechanism	Reference
Salmonella spp.	AvrA FliC	Increased incidence ratio and FliC-reactive antibodies in Dutch cohorts. Increased CRC risk after non-Enteritis or Typhimurium infections.	AvrA mediated colitis, activation of WNT/β-Catenin and STAT3 signaling pathways.	98,99,100,101,102,103
Pathogenic Escherichia coli spp.	Cif Cnf Cdt	EPEC detected in 55.9% of CRC patient biopsies, compared to 20.6% in healthy patient biopsies. Cif (7.9%), Cnf (36.7%), Cdt (8.2%) of CRC biopsies.	Activation of inflammatory signaling cascades, Cancer cell detachment and survival	26, 27, 104,105,106,107,108,109,110,111,112,113
Clostridium difficile	TcdB	Experimental validation of a carcinogenic strain from biofilm-positive fecal slurries	Increased WNT/β-Catenin signaling, pro-carcinogenic IL-17 mediated immune response	114
Klebsiella pneumoniae	Clb?	Experimental validation of tumorigenesis after infection in colitis-associated cancer models; mechanism unclear	Carcinogenic activity modulated by microbiome status	117
Citrobacter rodentium	UshA	Experimental validation, identification of UshA-induced mutational signature in CRC cases	DNA damage and mutagenesis after transient infection	118
Campylobacter jejuni	Cdt	Experimental validation of tumorigenesis after infection with a CRC clinical isolate	DNA damage	121

Abbreviations: colorectal cancer, (CRC); avirulence A, AvrA; flagellar structural protein, FliC; cycle inhibiting factor, Cif; cytotoxic necrotizing factor 1, Cnf1; cytolethal distending toxin, Cdt; Clostridium difficile Toxin B, TcdB; colibactin, Clb; UDP-sugar hydrolase, UshA; signal transducer and activator of transcription 3, STAT3; interleukin 17, IL-17.