bovis/gallolyticus plays

an etiological role in the development of colorectal tumors or it is merely a marker of the disease. There are many clues provide strong evidence for the etiological role of S. bovis/gallolyticus in colon cancer development. The striking association between bacteremia caused by S. bovis biotype I and both colonic neoplasia (71%) and bacterial endocarditis (94%), compared with bacteremias caused by the closely related organisms CP690550 such as S. bovis variant and S. salivarius, suggests the possibility of specific bacterium-host cell interaction involving S. bovis biotype I organisms [85]. Later, S. gallolyticus subspecies gallolyticus, rather than other closely related taxa, was found to be actively colonizing colorectal tumors and primarily associated with colorectal cancer [40]. In addition, these bacteria showed AZD0156 in vivo special predilection to colonic lesions rather than other members of group D Streptococcus endocarditis. It was found that of 77 infections with group D Streptococcus endocarditis, colonic polyps selleck kinase inhibitor and colonic carcinoma were

significantly more frequent in the S. bovis/gallolyticus group, 67 and 18%, than in the Enterococcus group, 21 and 2%, respectively [3]. Furthermore, the appearance of new colonic lesions within 2 to 4 years after the incidence of S. bovis/gallolyticus bacteremia/endocarditis provides clearer evidence that S. bovis/gallolyticus is not merely a consequence of the tumor lesion [86].

For this reason, patients with infectious endocarditis about and normal colonoscopy may be included in the group that presents risk for developing colonic cancer because of the late appearance of such lesions after the infectious episode of S. bovis/gallolyticus. In terms of pathogenesis, as S. bovis/gallolyticus is a transient normal flora in the gut, researchers have postulated that the increased load of S. bovis/gallolyticus in colon might be responsible for its association with colon cancer. Several studies showed increased stool carriage of S. bovis/gallolyticus in patients with inflammatory bowel diseases or malignant/premalignant lesions of the colon; around 56% of patients with S. bovis/gallolyticus bacteremia/endocarditis showed increased faecal carriage, when compared to normal subjects or patients with benign diseases of the colon, such as colonic diverticulosis, inflammatory bowel disease, cecal volvulus, perirectal abscess and hemorrhoids (10-23%) [2, 67, 75]. Another clue supporting the etiological role of S. bovis/gallolyticus, patients diagnosed with colon cancer have only 3-6% chance to develop S. bovis/gallolyticus bacteremia/endocarditis [87]; this is far lower than the percentage of the detection of colorectal cancer in patients with S. bovis/gallolyticus bacteremia/endocarditis, >70%. S. bovis/gallolyticus is shown to have indiscriminate pathogenic factors.