A case of infective endocarditis caused by Kocuria rosea in a non-compromised patient

Abstract

A 79-year-old male with no history of immunodeficiency was transferred to our hospital complaining of shortness of breath and general fatigue. He was diagnosed with recent myocardial infarction and underwent emergent percutaneous coronary intervention. However, the course of congestive heart failure was poor, and he required respiratory support and renal replacement therapy. Kocuria rosea was detected in blood culture obtained on admission, and then a follow-up echocardiogram revealed infective endocarditis. We administered ampicillin-sulbactam and performed urgent operation. The post-operative course was uneventful with 4-week administration of antimicrobial agents.

Learning objectives

Infective endocarditis caused by Kocuria rosea may also occur in non-compromised patients although K. rosea infections have been reported only in compromised hosts. This pathogen is sensitive to a variety of antibiotics. We selected ampicillin-sulbactam to treat infective endocarditis based on a sensitivity examination, and the patient's post-operative clinical course was uneventful. Ampicillin-sulbactam may be a useful treatment option.

Introduction

Kocuria rosea is a rare causative pathogen of infective endocarditis, and there are no defined regimens for this pathogen because of its rarity. There have been a few reports of infective endocarditis caused by K. rosea in compromised patients, most of whom were administered ceftriaxone, vancomycin, or gentamycin. We report a case of infective endocarditis in a non-immunodeficient patient, who was cured by multidisciplinary treatment with necessary and sufficient debridement and appropriate antimicrobials.

Case report

A 79-year-old male, who was previously healthy except for a history of chronic obstructive pulmonary disease, complained of shortness of breath and general fatigue, and was transferred to the emergency room of our hospital from his local clinic. He had been suffering from these complaints for 6 days before visiting the clinic. Physical examination revealed to and fro murmur in the right second intercostal area and coarse crackles on both sides. He had orthopnea and needed support by non-invasive ventilation although there were no signs of shock. Electrocardiogram showed an elevation of ST segment in V2 to V4, and laboratory blood testing revealed a significant increase of troponin I (1186.2 pg/ml) and creatine kinase (21 IU/l). In addition, brain natriuretic peptide was noticeably increased to 6701.1 pg/ml, white blood cell was 27,200/μl, and C-reactive protein was 34.6 mg/dl. Moreover, acute renal failure was observed at admission, and creatine was 1.95 mg/dl. A specific examination for immunodeficiency was carried out that was negative for human immunodeficiency virus infection. Leukocytes/neutrophils were elevated reflecting infection. Echocardiography showed deterioration of left ventricular (LV) wall motion, especially broad anterior wall, and ejection fraction was 52.5 %. We were not able to detect vegetation on the aortic valve or peri annular abscess on admission although we detected moderate aortic regurgitation. The LV end-diastolic diameter was 56 mm, and the LV end-systolic diameter was 40 mm. He was diagnosed as having congestive heart failure due to recent myocardial infarction and aortic regurgitation. He underwent coronary angiography and myocardial infarction was diagnosed due to sub-total occlusion of proximal left anterior descending artery (#6). The flow beyond that point was delayed, and there was also 50 % stenotic lesion on the proximal left circumflex branch (Fig. 1). Cardiologists performed percutaneous coronary intervention to #6 using a drug-eluting stent immediately. Although recanalization was obtained, we could not control heart failure even with catecholamine use, non-invasive ventilation, and renal replacement therapy. Seven days after admission, follow-up echocardiography showed worsening aortic regurgitation and vegetation attached to the aortic valve (Fig. 2). Blood culture obtained on admission revealed bacteremia due to K. rosea, which was identified by Vitek 2 ID-GPC card (bioMérieux Japan Ltd., Tokyo), and the patient was diagnosed as having infective endocarditis. Immediately after diagnosis, ampicillin-sulbactam (3 g 6 hourly) was started according to antibiotics sensitivity (Table 1) and urgent operation was performed. Intraoperative findings revealed the destroyed aortic valve and aortic peri annular abscess (Fig. 3A). We performed aortic valve replacement with aortic annular reconstruction using a bovine pericardial patch (Fig. 3B). Post-operative course was uneventful with 4-week antibiotic administration. Post-operative echocardiography showed no perivalvular regurgitation or signs of aortic peri annular abscess.

Fig. 1.

Coronary angiography. Coronary angiography showed sub totally occluded left anterior descending artery (A). The distal of the left anterior descending artery was contrasted late (B, arrow).

Fig. 2.

Pre-operative echocardiography. Pre-operative trans-thoracic echocardiography in the apical three-chamber view showed vegetation attached to the aortic valve (white arrow head). (A: systolic phase; B: diastolic phase).

Table 1.

The drug sensitivity for Kocuria rosea.

Antibiotics	Sensitivity	Minimum inhibitory concentration (μg/ml)
Penicillin	Sensitive	≦0.0
Ampicillin	Sensitive	≦0.2
Amoxicillin	Sensitive	≦0.2
Piperacillin	Sensitive	≦0.2
Cefazolin	Sensitive	0.5
Ceftazidime	Resistant	>2
Ceftriaxone	Sensitive	1
Cefozopran	Sensitive	0.5
Cefmetazole	Resistant	2
Cephalexin	Sensitive	≦1
Imipenem-cilastatin	Sensitive	≦0.1
Ampicillin-sulbactam	Sensitive	≦0.1
Piperacillin-tazobactam	Sensitive	≦0.1
Azithromycin	Sensitive	≦0.5
Clindamycin	Sensitive	≦0.2
Minomycin	Sensitive	≦0.5
Levofloxacin	Resistant	>4
Teicoplanin	Sensitive	≦0.2
Trimethoprim-sulfamethoxazole	Sensitive	≦5

Fig. 3.

Intraoperative findings. The aortic valve was destroyed intensely due to vegetation, and aortic peri annular abscess was formed (A, arrow head). We performed extended debridement of the aortic annulus and reconstructed it with a bovine pericardial patch (B, arrow).

Discussion

We encountered a case of infective endocarditis caused by K. rosea in a non-immunodeficient patient. Kocuria rosea is a rare causative pathogen organism of infective endocarditis, and infective endocarditis caused by this organism mostly occurs in immunocompromised patients. Specific antibiotic therapy for K. rosea is yet to be controversial.

This case highlighted the following two findings. Kocuria rosea can be a causative organism in patients without immunodeficiency, and infective endocarditis due to this pathogen can be treated with ampicillin-sulbactam.

First, K. rosea can be a causative organism in patients without immunodeficiency. Kocuria rosea is considered an atypical pathogen for infective endocarditis, and there are a few reports of infective endocarditis due to this pathogen [1], [2], [3]. Previous reports have suggested that infections by Kocuria species including K. rosea are more likely to occur in immunocompromised patients [4] or patients with comorbidities [2]. In the current case, the blood culture revealed bacteremia, and echocardiography showed vegetation of the aortic valve although immunodeficiency was not detected. When blood cultures show bacteremia due to K. rosea, the possibility of infective endocarditis due to K. rosea may be considered, even in patients who are not immunocompromised.

Second, ampicillin-sulbactam may be effective for the treatment of infective endocarditis caused by K. rosea. However, there are no clearly defined antimicrobial regimens for infective endocarditis caused by this pathogen. Antimicrobial agents are selected based on susceptibility tests or by referring to previous reports. It was reported previously that K. rosea is sensitive to amoxicillin-clavulanic acid, ceftriaxone, amikacin, and doxycycline [2]. Gunaseelan et al. [2] treated infective endocarditis due to K. rosea with administration of vancomycin for 14 days and ceftriaxone for 4 weeks. In this report, infective endocarditis was treated with antimicrobials only, and vegetation disappeared. We decided to administer ampicillin-sulbactam in this case because of its susceptibility to pathogens and because amoxicillin-clavulanic acid has previously been reported to be an effective antimicrobial agent for the treatment of infective endocarditis [4]. In addition, the duration of antimicrobial administration is not defined clearly for this pathogen. In a previous report, the duration of antimicrobial therapy was 4 weeks with gentamycin and ceftriaxone [3]. Guidelines for prevention and treatment of infective endocarditis published by the Japanese Circulation Society in 2017 recommend that the duration of antimicrobial administration for native valve endocarditis should be 4 to 6 weeks, although there are no descriptions of K. rosea [5]. We administered antimicrobial agents for 4 weeks with regular echocardiographic follow-up, and the patient recovered well without recurrence and mycotic coronary aneurysms (MCA). MCA are a known complication of infective endocarditis [6]. They are caused by embolization of vegetation or direct bacterial invasion. In this case, intravascular ultrasound was not performed, but since angiography showed irregular stenosis and atherosclerotic changes in other coronary arteries, we concluded that the coronary artery stenosis was due to atherosclerosis. However, since the possibility of vegetation embolization could not be completely ruled out, careful follow-up was considered because of the possibility of the development of MCA.

Further research and experience are required to determine the optimal regimen for infective endocarditis due to K. rosea in the future.

Declaration of competing interest

The authors declare that there is no conflict of interest.