Multivalvular infective endocarditis due to streptococcus pluranimalium in a young patient with bicuspid aortic valve

Abstract

Multivalvular infective endocarditis (MIE) is an uncommon condition associated with increased morbidity and mortality compared to single-valve involvement. We present the case of a young patient with a bicuspid aortic valve and MIE affecting both the aortic and mitral valves, caused by Streptococcus pluranimalium. Timely diagnosis, targeted antibiotic therapy, and surgical intervention with dual-valve replacement led to a favorable clinical outcome. This case highlights the importance of considering the diagnosis of infective endocarditis in young patients presenting with fever and constitutional symptoms without an apparent cause and initiating the investigation of an underlying congenital heart disease. It also highlights that uncommon pathogens may be etiological agents of infective endocarditis in patients with predisposing valvular abnormalities.

Introduction

Infective endocarditis (IE) is an active infection within the heart, typically caused by bacteria. Its hallmark is the formation of vegetations, which may develop on one or more heart valves —whether native or prosthetic— as well as on the chordae tendineae, endocardial surface, intracardiac devices, or even the intimal layer of large vessels [1]. The involvement of two or more valves, known as multivalvular infective endocarditis (MIE), is relatively uncommon, with incidence ranging from 12% to 30%. MIE may result from simultaneous infection of two previously damaged valves in the presence of persistent bacteremia, or more commonly, from sequential seeding of a previously damaged valve. MIE generally leads to a worse prognosis compared to cases where only one heart valve is affected [2, 3]. Approximately 5% to 25% of patients with infective endocarditis present with cutaneous manifestations, including purpura, Osler’s nodes, Janeway lesions, and conjunctival hemorrhages [4].

We present the case of a 29-year-old man with a two-week history of fever and general symptoms, in whom a thorough physical examination—including the identification of Janeway lesions, Osler nodes, and murmurs in the aortic and mitral areas—guided the diagnosis toward infective endocarditis and prompted investigation for an underlying congenital heart disease.

Case report

Diagnostic work-up

A 29-year-old man presented with weakness, fatigue, muscle pain, joint pain, nausea, and fever, evolving over two weeks. He had undergone endodontic treatment one month prior to symptom onset. On physical examination, Janeway lesions and an Osler node were identified (Fig. 1), along with a diastolic murmur at the aortic focus and a systolic murmur at the mitral focus, raising suspicion for infective endocarditis (IE).

Figure 1.

Red arrow shows Osler node and blue arrows show Janeway lesions in the palmar region.

Laboratory tests revealed leukocytosis and blood cultures grew Streptococcus pluranimalium (Table 1). A transthoracic echocardiogram revealed a calcified vegetation (14x7 mm) attached to a bicuspid aortic valve, causing a double valvular lesion with predominant stenosis, and a calcified vegetation (10x15 mm) on the anterior leaflet of the mitral valve. The patient met Duke criteria for IE, in accordance with the International Society of Cardiovascular Infectious Diseases and the 2023 ESC Guidelines for the management of infective endocarditis [5, 6].

Table 1.

Laboratory tests.

	Value	Reference Value
Blood chemistry
Glucose, mg/dL	96	70–105
Albumin, mg/dL	2.9	3.4–5
Alanine aminotransferase, UI/L	38	13–40
Aspartate aminotransferase, UI/L	36	15–48
Total Bilirubin, mg/dL	1.1	0.2–1
Lactate dehydrogenase, UI/L	321	180–250
Kidney Function
Creatinine, mg/dL	1.1	0.5–0.9
Complete Blood Count
Hemoglobin, g/dL	12.1	12–18
Hematocrit, %	36.3	37–52
Leukocytes, K/mL	13.0	4.5–10
Neutrophils, K/mL	10.0	3.0–6.9
Lymphocytes, K/mL	2.3	0.6–3.4
Platelets, K/mL	243	150–400
Coagulation Tests
Prothrombin time, s	14.4	11–15
Partial thromboplastin time, s	30.7	30–40
Microbiology
Blood cultures	Streptococcus pluranimalium	Without bacterial growth

Additional imaging ruled out aortic coarctation, aortic dilation, and cerebrovascular malformations.

Therapeutic interventions

Empiric treatment was initiated with intravenous ceftriaxone (2g every 12hours for 21 days). Given the extent of valvular involvement, the patient subsequently underwent surgical replacement of both the aortic and mitral valves.

Histopathological analysis of the excised vegetations confirmed the presence of bacterial colonies, fibrin, dystrophic calcification and inflammatory infiltrates.

Follow-up

The patient had an uneventful postoperative course and was discharged without complications. No adverse events or sequelae were noted at discharge, suggesting a favorable short-term clinical outcome. Continued clinical and echocardiographic monitoring was planned to ensure long-term valve function and absence of relapse.

Discussion

IE is defined as an infection of the endocardium and valves of the heart. IE is one of the most serious infectious diseases, with an in-hospital mortality of 20%–25%. The prognosis can worsen when there is involvement of multiple heart valves, increasing the mortality to 56% [2, 7]. A recent cohort study revealed that MIE accounts for one-seventh of all IE cases and can affect both prosthetic and native valves [2]. Congenital heart diseases (CHD) are one of the main risk factors for the development of EI in native valves and the bicuspid aortic valve (BAV) is the most common form of CHD, with a prevalence of 0.5%–2.0% [8]. In our patient, a bicuspid aortic valve was identified. In our patient, mitralaortic involvement could have resulted from one of the following three mechanisms: 1) Damage and infection of the anterior mitral valve leaflet due to a jet lesion secondary to aortic insufficiency (the most common), 2) Local dissemination of infection from aortic endocarditis with formation of an anterior abscess in the intervalvular fibrous body, resulting in secondary destruction of the mitral annulus with or without associated mitral insufficiency, or 3) ‘Kissing’ vegetation mechanism in the mitral valve, which occurs due to contiguous spread of infection from large vegetations on the non-coronary cusp of the aortic valve, prolapsing into the left ventricular outflow tract during diastole and coming into contact with the ventricular surface of the adjacent anterior mitral valve leaflet, thereby initiating local infection [3]. There are rare pathogens that cause IE, such as S. pluranimalium, a bacterium originally described in animals, which has been reported in rare cases of infection in humans. Affected patients often have predisposing factors such as congenital or acquired heart disease, intravenous drug use, immunosuppression or contact with animals. Described cases include mitral endocarditis with brain abscess in an adolescent [9] and pneumonia with pleural effusion in a patient with exposure to animals [10].

Patients with MIE are at higher risk of developing heart failure due to more extensive tissue destruction. It is estimated that around 85% of patients with MIE require surgical treatment, compared to those with only one affected valve. Regarding surgical indications, the ESC Guidelines for the management of infective endocarditis maintain the following main criteria: heart failure secondary to severe valvular dysfunction, uncontrolled infection (presence of abscesses, persistence of bacteremia, particularly virulent microorganisms such as S. aureus or S. pluranimalium), and prevention of embolisms in the presence of large vegetations (>10 mm), especially if there are previous embolic events [6]. However, it has been observed that only 56% of patients receive this treatment, which could impact mortality [2].

Conclusion

Our case highlights the development of MIE caused by S. pluranimalium in a young patient with a bicuspid aortic valve. The key clinical points of our report are as follows: (1) In any young patient presenting with fever and constitutional symptoms of unclear origin, IE should be considered in the differential diagnosis; (2) in Young individuals, it is important to identify any underlying CHD; (3) microbiological isolation is essential for guiding appropriate antimicrobial therapy, which, when combined with surgical intervention, can significantly improve outcomes; (4) to our knowledge, this is the first reported case of MIE caused by S. pluranimalium, a pathogen more commonly isolated in the pediatric population.

Summary Table
Domain	Findings/Data
Patient demographics	29-year-old male
Chief complaints	Weakness, fatigue, muscle and joint pain, nausea, fever
History	Endodontic treatment 1 month prior to symptoms
Vital signs	Febrile (102.2 °F)
Physical exam	Janeway lesions, Osler node, diastolic murmur (aortic), systolic murmur (mitral)
Microbiology	Blood cultures positive for Streptococcus pluranimalium
Echocardiograpy	- Vegetation on bicuspid aortic valve (14x7 mm), causing stenosis—Vegetation on anterior mitral leaflet (10x15 mm)
Other Imaging	No aortic coarctation, dilation, or cerebral vascular malformations
Histopathological analysis	Presence of bacterial colonies, fibrin, dystrophic calcification and inflammatory infiltrates.
Diagnosis	Infective endocarditis (IE), confirmed by Duke criteria and ESC 2023 guidelines

Conflict of interest

The authors declare no conflict of interest.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical approval

No ethical approval was required for this article.

Consent

Written informed consent was obtained from the patient to publish this report in accordance with the journal’s patient consent policy.

Guarantor

Ana Lilia Peralta-Amaro.