Nihita Manem, BS, David Miller, BS, Debra Tristram, MD, Michael Tadros, MD, MPH, FACG; Albany Medical Center, Albany, NY
Introduction: The incidence of colorectal cancer (CRC) increases with concurrent bacterial infections, especially Streptococcus bovis. It is unclear whether S. bovis has a carcinogenic effect via toxic byproducts and chronic inflammation or if the invasive cancer leads to disruptions in colonic mucosa and subsequent bacterial translocation. We report a case that sheds light on the underlying disease pathogenesis.
Methods: A 55-year-old male without significant past medical history presented with syncope and septic shock. Patient denied abdominal complaints and bowel habit changes. Labs were significant for leukocytosis and mild iron deficiency anemia. Blood culture indicated a S. bovis infection. An echocardiogram revealed vegetations on aortic and mitral valves. A prior colonoscopy done 4 years ago showed advanced adenomas. Repeat colonoscopy revealed a 1 cm scirrhous-like, ulcerated mass in the cecum burrowing into a fold. Biopsy showed moderately differentiated adenocarcinoma. After medical stabilization, the patient underwent a laparoscopic right hemicolectomy. There was no lymph node involvement. Discussion: S. bovisbacteremia is associated with a 7-fold increase in CRC development. Literature reports a variable degree of association: 18-62% of patients with S. bovisinfective endocarditis had colorectal tumors. However, the pathophysiology of S. bovis and CRC is unclear.
S. bovis adheres to intestinal cells and can grow in bile, allowing hepatic filtration bypass. S. bovishas a high affinity for matrix proteins at injury sites, such as heart valve vegetations or tumors. The pili of S. bovisallows attachment and plays a role in the generation of biofilm on damaged tissues, including heart valves and precancerous lesions.
This case study proposes an underlying association between S. bovis and CRC (Figure 2). Given the patient’s history of advanced adenomas, the cancer most likely developed first. The CRC disrupted mucosal barriers, increasing the likelihood of a S. bovis invasion into tissues. A subsequent inflammatory reaction increased epithelial permeability, leading to S. bovis bacteremia. Because S. bovis has a high affinity for the cardiac endothelium, it most likely formed biofilms on the patient’s aortic and mitral valves, explaining the echocardiogram findings. Our hypothesis is supported by the small tumor size and lack of lymph node involvement. In this case, S. bovis infective endocarditis developed because of the CRC rather than due to the carcinogenic effects of S. bovis.
Figure 1. Endoscopic finding of cecal cancer
Figure 2. Proposed mechanism for S. Bovis caused by CRC
Disclosures: Nihita Manem indicated no relevant financial relationships. David Miller indicated no relevant financial relationships. Debra Tristram indicated no relevant financial relationships. Michael Tadros indicated no relevant financial relationships.