Streptococcus bovis endocarditis secondary to colorectal cancer: A case report

Abstract

BACKGROUND

Streptococcus bovis (S. bovis) bacteremia and infective endocarditis have a well-established association with colorectal cancer (CRC), though the mechanisms underlying this potentially bidirectional relationship remain poorly understood.

CASE SUMMARY

This case report describes a 55-year-old male with a history of hypertension and hemicolectomy due to advanced colorectal adenomas who presented with syncope, septic shock, and a 12-pound weight loss over 3 weeks. Subsequent blood cultures grew S. bovis, with a transthoracic echocardiogram revealed mobile vegetations on both the aortic and mitral valves. A sessile, non-obstructing cecal adenocarcinoma was also observed on colonoscopy. The patient was started on 6 weeks of intravenous ceftriaxone, followed by surgical repair of both heart valves and a laparoscopic right hemicolectomy.

CONCLUSION

This presentation underscores how CRC-induced mucosal disruption may predispose to bacterial translocation, resulting in systemic infection and endocarditis.

Key Words: Streptococcus bovis; Colorectal carcinoma; Endocarditis; Inflammation; Bacteremia; Case report

Core Tip: This case report illustrates the well-recognized but still poorly understood link between Streptococcus bovis (S. bovis) infection and colorectal cancer (CRC). By detailing a patient who developed S. bovis bacteremia and dual-valve endocarditis in the setting of a small, localized cecal adenocarcinoma, the case provides insight into how early mucosal disruption from CRC may facilitate bacterial translocation and systemic infection. The report underscores the necessity of prompt colorectal evaluation in all patients with S. bovis bacteremia-even without gastrointestinal symptoms-and highlights the potential role of S. bovis both as a biomarker and a participant in CRC pathogenesis.

INTRODUCTION

Colorectal cancer (CRC) remains a significant health burden in the United States, serving as the third-most diagnosed cancer in both men and women, as well as the second leading cause of overall cancer death. While obesity, physical inactivity, and low-fiber, highly processed diets have previously been highlighted as risk factors, the molecular pathogenesis is highly variable, which contributes to differing prognostic and treatment guidelines[1]. The two principal pathways implicated in CRC development are the chromosomal instability (CIN) pathway and the microsatellite instability (MSI) pathway. The CIN pathway involves sequential mutations in the APC, KRAS, and TP53 genes, ultimately leading to unchecked cellular proliferation and resistance to apoptotic signaling. This series of mutations is known as the traditional adenoma-carcinoma sequence and accounts for 70%-90% of CRC cases[2-4]. In contrast, the MSI pathway describes either the inherited or epigenetic loss of DNA mismatch repair genes, allowing for the accumulation of pro-carcinogenic mutations. This pathway, otherwise known as the serrated neoplasia sequence, results in the development of serrated precursor lesions, including sessile serrated adenomas and traditional serrated adenomas, and accounts for 10%-20% of CRC cases[5,6].

Streptococcus bovis (S. bovis), which belongs to the group D Streptococci family, represents a normal component of the gut microbiome, and is classically linked to endocarditis and bacteremia[7]. A clinically significant association exists between S. bovis infection and CRC, as up to 80% of patients with S. bovis infection are found to have concurrent colonic neoplasms upon endoscopic evaluation, ranging from adenomas to invasive carcinomas[8]. This relationship may be bidirectional, with S. bovis patients being at higher risk of harboring CRC, in addition to CRC patients being more susceptible to S. bovis colonization, suggesting a possible role in CRC tumorigenesis[8,9].

It remains unclear whether S. bovis fosters a carcinogenic environment through mechanisms like toxic byproducts and chronic inflammation, or if CRC-induced disruptions in colonic mucosa increase susceptibility to preferential bacterial translocation. To that end, we report a case that offers insight into underlying disease pathogenesis.

CASE PRESENTATION

Chief complaints

A 55-year-old male presented to the emergency department with syncope, septic shock, and a 12-pound weight loss over the past three weeks.

History of present illness

The patient developed syncope and stated that he has been able to tolerate only minimal amounts of food and fluids.

History of past illness

The patient has a past medical history of hypertension, asthma, bipolar disorder, bowel replacement, and colon cancer status post-hemicolectomy.

Personal and family history

The patient is a non-smoker and non-drinker. He has a family history of an unknown cancer in his mother, as well as colon cancer in his aunt and uncle. He does not regularly follow-up with his primary care provider, and his last colonoscopy was three years prior.

Physical examination

The patient was 167 cm tall and weighed 97 kg. On admission, the patient was tachycardic with a heart rate of 97 beats per minute, blood pressure of 106/63 mmHg (14.1/8.4 kPa), respiratory rate of 20/minute, oxygen saturation of 95%, and body temperature of 36.8 °C. Physical examination revealed mild epigastric discomfort to deep palpation without guarding or rigidity. No other physical abnormalities were detected.

Laboratory examinations

Laboratory evaluation was notable for initial leukocytosis and microcytic anemia, in addition to hypoproteinemia, hypocalcemia, and mild hyperglycemia (Table 1).

Table 1 Key laboratory blood findings on admission.

Parameter	Result	Reference range	Interpretation
WBC	5.1 × 103/µL (initial 185)	3.9-10.6 × 103/µL	Initially high, normalized
Hemoglobin	9.2 g/dL	13.5-17.0 g/dL	↓
Hematocrit	27%	41%-53%	↓
Platelets	225 × 103/µL	130-400 × 103/µL	Normal
Sodium	139 mEq/L	135-145 mEq/L	Normal
Potassium	3.6 mEq/L	3.5-5.0 mEq/L	Normal
BUN	3 mg/dL	6-22 mg/dL	↓
Creatinine	0.67 mg/dL	0.60-1.30 mg/dL	Normal
Calcium	8.3 mg/dL	8.5-10.5 mg/dL	↓
Total protein	5.3 g/dL	6.0-8.0 mg/dL	↓
Glucose	103 mg/dL	65-99 mg/dL	Slight ↑

WBC: White blood cells, BUN: Blood urea nitrogen.

Imaging examinations

Standard blood culture panels grew S. bovis. A transthoracic echocardiogram demonstrated mobile vegetations on both the aortic and mitral valves, consistent with infective endocarditis. Given the S. bovis bacteremia, gastroenterology was consulted. Colonoscopy revealed a 1 cm fungating, sessile, ulcerated, non-obstructing mass in the cecum, appearing scirrhous-like and depressed centrally. Biopsy showed moderately differentiated adenocarcinoma with 1.2 cm submucosal invasion and no lymph node involvement (Figure 1).

Figure 1 Endoscopic image of a 1 cm ulcerated, polypoid mass in the cecum, later confirmed as moderately differentiated adenocarcinoma.

FINAL DIAGNOSIS

A diagnosis of S. bovis infection with concurrent colorectal adenocarcinoma was established.

TREATMENT

The patient was started on intravenous ceftriaxone for 6 weeks, per Infective Endocarditis guidelines. Cardiothoracic surgery performed a repair of both aortic and mitral valves. Following stabilization, he underwent laparoscopic right hemicolectomy on the same day, which revealed negative margins and no nodal spread.

OUTCOME AND FOLLOW-UP

His recovery was uneventful, and he was discharged on postoperative day 5 with follow-up in cardiology and gastroenterology clinics.

DISCUSSION

S. bovis, a bacterial strain that is a component of healthy gut flora, elicits an eight-fold increase in CRC development. Prior research has found that 51% of patients with S. bovis bacteremia had concurrent adenocarcinoma, with the most common site of malignancy in the sigmoid colon. Similarly, literature reports that 18%-62% of patients with S. bovis infective endocarditis had colorectal tumors[7-9]. Despite this well-established link, the pathophysiology underlying the relationship between S. bovis and CRC is poorly understood.

S. bovis not only exhibits adhesive properties, allowing the bacteria to colonize intestinal cells, but also uniquely grows in bile, unlike many of its alpha-hemolytic streptococci counterparts[10]. Furthermore, its ability to bypass filtration by the hepatic reticulo-endothelial system accelerates its entry into the systemic circulation[11]. S. bovis also displays a high affinity for extracellular matrix proteins, particularly type 1 collagen, which is abundantly expressed at sites of tissue injury, remodeling, or inflammation, such as heart valve vegetations and tumors[12,13]. In bacteremia, S. bovis utilizes pili to attach to mucosal epithelial cells for ease of translocation, ultimately facilitating formation of biofilm on damaged heart valves and precancerous epithelium[12-14].

This case study proposes a novel pathogenetic mechanism between S. bovis and CRC. (Figure 2). Given the patient’s history of advanced adenomas, it is likely that the invasive cancer developed first and the CRC-induced disruption in mucosal protective barriers subsequently increased susceptibility of a S. bovis invasion into tissues. In response to tumor-related injury, immune activation triggered the release of pro-inflammatory mediators, further increasing epithelial permeability and leading to bacteremia. As S. bovis displays a notable predilection for the cardiac endothelium, it most likely formed biofilms on the patient’s aortic and mitral valves, which ultimately manifested as the vegetations observed on echocardiogram findings. Our hypothesis is supported by the small tumor size and the absence of lymph node involvement, suggesting an early-stage malignancy with localized disruption of the mucosal barrier.

Figure 2 Proposed mechanism for Streptococcus bovis bacteremia caused by colorectal cancer.

In this patient, the systemic infection ultimately necessitated dual valve repair and right hemicolectomy. His favorable recovery following antibiotic therapy, valve repair, and tumor resection further supports a model in which colorectal malignancy preceded bacterial invasion, with management targeting both the infectious complication and the underlying neoplastic source. Notably, prior research has hypothesized an etiological role of S. bovis in the neoplastic transformation of colonic mucosa, whether through an increased inflammatory load or pili attachment to precancerous colonic lesions[15,16]. To that end, this relationship is likely bidirectional; the presence of one condition may exacerbate or facilitate the presence of the other, highlighting a complex interplay in which CRC and S. bovis infection may mutually enforce disease progression.

CONCLUSION

This case highlights the complex and tightly bidirectional relationship between S. bovis and CRC. While S. bovis infection has been widely recognized as a clinical marker warranting colorectal evaluation, this case supports a sequence in which colorectal adenocarcinoma preceded the onset of bacteremia and infective endocarditis. The patient’s history of advanced adenomas and the subsequent development of a small, localized, non-obstructing cecal tumor with no lymph node involvement suggests that insult to the mucosal barrier by malignancy may have facilitated translocation of S. bovis into the bloodstream. This report reinforces the importance of prompt gastrointestinal evaluation in all patients with S. bovis bacteremia, even in the absence of overt gastrointestinal symptoms, as early detection of potential colorectal neoplasia can significantly impact treatment outcomes. Furthermore, these findings add to the growing body of evidence proposing that S. bovis may serve as both a biomarker and facilitator of disease progression. Further research is needed to fully elucidate the causative vs opportunistic role of S. bovis in colorectal carcinogenesis, as well as explore its potential for both preventative and therapeutic intervention.