Infective endocarditis (IE) is a serious and potentially life-threatening condition characterised by microbial infection and inflammation of the endocardial surface, most commonly involving cardiac valves [1]. The epidemiology of IE has been evolving, with an overall incidence of 1.5–9.6 per 100,000 people, and rising rates among elderly patients, those with prosthetic valves [0.5–3.1% per patient-year after transcatheter aortic valve implantation (TAVI)], cardiac implantable devices (now up to 10% of IE cases), and healthcare-associated settings (34% of cases) [2]. The diagnostic standard is the modified Duke criteria, which integrate major findings from blood cultures and echocardiography with various minor criteria to confirm infective endocarditis. Treatment consists of prolonged courses of intravenous antibiotics and often requires surgical intervention [3]. IE continues to carry substantial morbidity and mortality, even with modern diagnostic and therapeutic advances. While neurological and renal manifestations of IE are well-documented, gastrointestinal involvement is less commonly reported [3].

Gastrointestinal manifestations, while relatively rare, can include splenic infarction, hepatosplenic abscesses, mesenteric ischaemia and gastrointestinal bleeding secondary to embolic or immune-mediated mechanisms [3]. These symptoms may be the presenting complaint of the patient. Without awareness of the association between IE and gastrointestinal manifestations, the diagnosis and treatment of this condition can be delayed, leading to worse outcomes.

We present a case of a 34-year-old male patient who initially presented with unexplained gastrointestinal symptoms—fever, weight loss and change in bowel habit (frequent bloody diarrhoea with tenesmus and mucus). There was an absence of detectable intestinal pathology on colonoscopy and subsequent findings revealed a link between the gastrointestinal symptoms and IE-related complications.

IE presenting as clinical colitis has not previously been described in the literature. Whilst a link between Streptococcus gallolyticus (formerly Strep.bovis) IE and colonic neoplasms have been well-described [4], our case describes a link between IE and gastrointestinal symptoms without macroscopic colonic pathology.

Following the course of antibiotics, the patient’s symptoms considerably improved. He was discharged to the endocarditis clinic for close monitoring. From a cardiac and infective perspective, he was asymptomatic and inflammatory markers remained low (Fig. 3)—because of this, further microbiological testing was not attempted. The patients index left ventricular ejection fraction at presentation was 60%, there was no decrease on subsequent examinations. Echocardiography six months after presentation (Fig. 4), revealed persisting severe mitral regurgitation with an eccentric jet (regurgitant volume 66 mL), which persisted at a 20-month follow-up (Fig. 5). He continues to be closely monitored and will be evaluated as an outpatient for possible mitral valve repair/replacement.

Fig. 3.

Trend in C-reactive protein. Trend in C-reactive protein during inpatient admission and treatment with intravenous antibiotics. This diagram was generated by the programme cerner.

Fig. 4.

Transthoracic echocardiography (TTE) 6 months from index admission. TTE with residual mitral valve regurgitation and echogenic structure connected to the mitral valve.

Fig. 5.

Transoesophageal echocardiography (TOE) 20 months from index admission. Top left: 4-chamber view demonstrates persistent mitral regurgitation. Top right: alternative 2D plane with colour doppler confirming a turbulent regurgitant jet directed into the left atrium. Bottom left: cross-sectional (short-axis) view with colour doppler showing the regurgitant jet spreading within the atrium. Bottom right: TOE 3D reconstruction displaying persistent mitral regurgitation.

Extra-cardiac symptoms are common in IE, and this is one of the reasons diagnosis is often delayed. In this case, the patient initially presented with gastrointestinal symptoms, including fever, weight loss and bloody diarrhoea. These symptoms prompted colonoscopic evaluation to rule out colitis.

The pathophysiology of gastrointestinal involvement in IE is multifactorial. Embolic phenomena, immune complex deposition and vasculitic processes can all contribute to the development of gastrointestinal symptoms [5, 6, 7]. In this case, the presence of renal infarcts and splinter haemorrhages helped confirm the diagnosis of IE with systemic involvement.

While the association between Streptococcus gallolyticus (formerly Strep.bovis) endocarditis and colonic neoplasia is well established [4], such cases typically involve identifiable colonic lesions serving as a portal of entry. In contrast, our patient presented with gastrointestinal symptoms without macroscopic colonic pathology, and blood cultures were negative. This suggests an alternative mechanism, potentially related to microinfarction or vasculitic phenomena secondary to embolic complications of IE.

The prompt initiation of appropriate antibiotic therapy was crucial in managing this patient. Intravenous amoxicillin, flucloxacillin and gentamicin were administered. The resolution of both cardiac and gastrointestinal symptoms with antibiotics underscored the link of IE with the gastroenterological symptoms, which may have been caused by colonic microinfarcts or vasculitis [8].

In this case, a causative bacteria was never identified. This is due to the fact that the patient had already received intravenous antibiotics empirically to treat presumed intraabdominal sepsis. Three doses of intravenous co-amoxiclav were given prior to any blood cultures being taken. A broad differential should be considered in the absence of a causative organism. HACEK organisms—Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella species—are well-known causes of endocarditis and may require prolonged culture incubation. In this case, the patient responded promptly to antibacterial therapy and further evaluation was not deemed to be of benefit.

The major strength of this case is the multidisciplinary team approach and long-term follow-up, which permitted an accurate correlation between systemic manifestations and cardiac disease. However, a significant limitation is that gastrointestinal involvement was not histologically confirmed by biopsy because of the patient’s clinical improvement with antibiotics.

This case underscores the need for increased awareness among healthcare providers regarding the diverse clinical presentations of IE. Clinicians should consider IE in patients presenting with unexplained gastrointestinal symptoms, particularly in the absence of detectable colonic lesions, ensuring a comprehensive evaluation is performed including a thorough cardiac examination. Recognising IE’s extracardiac manifestations, such as gastrointestinal involvement, can facilitate early diagnosis, appropriate treatment, and a multidisciplinary approach involving specialities such cardiology, infective diseases and gastroenterology. This can help prevent complications, such as embolic events, and improve patient outcomes.

To ensure comprehensive reporting, this case report was structured according to the case report (CARE) statement guidelines available on the CARE website. The CARE checklist has been provided as Supplementary Material.

• Infective endocarditis can cause a range of extra-cardiac manifestations, including abdominal pathology such as splenic infarct, hepatosplenic abscess, mesenteric ischaemia and gastrointestinal bleeding.

• Perform a thorough cardiac examination and consider infective endocarditis as a potential underlying cause in patients with unexplained gastrointestinal symptoms.

• If considering infective endocarditis, prompt collection of blood cultures prior to antibiotic administration can aid diagnosis and treatment.

The datasets generated or analysed during this case report are available from the corresponding author on reasonable request.

RA drafted the manuscript, performed a literature review, and collected clinical data. MZ contributed to echocardiographic analysis, and clinical interpretation. NK contributed to clinical interpretation. DK contributed to echocardiographic analysis, and clinical interpretation. DL contributed to the conception and design of the case report and supervised the project. All authors contributed to revising the manuscript critically for important intellectual content. All authors read and approved the final manuscript. All authors have participated sufficiently in the work and agreed to be accountable for all aspects of the work.

Written informed consent has been acquired from the patient for publication of this case and any accompanying images.

The authors sincerely thank the patient for their cooperation and consent to share their clinical case.

This research received no external funding

The authors declare no conflict of interest.

Supplementary material associated with this article can be found, in the online version, at https://doi.org/10.31083/BJHM52972.